Renal Dosing & Dialyzability
The dosing reference
Creatinine-clearance thresholds and dialyzability for 220 agents — the practical bedside questions: does the dose change in renal impairment, and is the drug removed by dialysis? Every row links back to its citation-grounded profile.
220 of 220 agents
| Agent | Renal dose adjustment | Dialyzable |
|---|---|---|
| 5-Fluorouracil TMA Pyrimidine analog | No standard CrCl-based dose adjustment for IV 5-FU (catabolism is enzymatic via DPD, not renal); dose by toxicity and consider DPYD-genotype-guided reduction. In significant renal impairment, monitor closely but renal clearance is a minor pathway. | — 5-FU has a very short half-life and is enzymatically catabolized; it is not managed by dialysis. Its catabolite fluoro-beta-alanine is renally excreted and can accumulate in renal failure but is not the toxic species. |
| Abemaciclib PSEUDO CDK4/6 inhibitor | No dose adjustment for mild-to-moderate renal impairment; severe renal impairment and ESKD are not well characterized (hepatic, not renal, impairment drives reduction). Critically, the drug-induced serum-creatinine rise should NOT trigger dose reduction by itself — verify true GFR first. | — Not characterized; abemaciclib is highly protein-bound and hepatically (CYP3A4) metabolized, so it is unlikely to be appreciably dialyzed. No ESKD dosing guidance exists. |
| Abiraterone LYTE CYP17 inhibitor | No formal renal dose adjustment for mild–moderate impairment (not studied in severe CKD/ESKD). Hepatic impairment requires dose reduction. The actionable adjustment is glucocorticoid coverage and potassium/BP management, not renal dosing. | Yes Highly protein-bound (>99%) and hepatically metabolized (CYP3A4/SULT2A1); not meaningfully dialyzable. No specific ESKD dosing established — manage electrolytes clinically. |
| Acalabrutinib HTN BTK inhibitor | No dose adjustment for mild-to-moderate renal impairment (CrCl ≥30 mL/min); severe impairment (CrCl <30) and dialysis are not well studied. <2% renal excretion; hepatic (CYP3A) clearance dominates. Acid-reducing agents alter absorption of the original capsule (a key non-renal interaction). | Yes Not meaningfully dialyzable — highly protein-bound, hepatically cleared small molecule. No post-HD supplemental dosing needed. |
| Adagrasib PRE KRAS G12C inhibitor | No dedicated renal dose adjustment is established; standard is 600 mg orally twice daily, modified for GI/QTc/hepatic toxicity. A measured (rather than creatinine-estimated) GFR is preferred when dosing renally cleared co-medications, because adagrasib inflates serum creatinine. | — Not characterized; highly protein-bound, hepatically metabolized (CYP3A4) small molecule, unlikely to be appreciably dialyzed. No ESKD dosing guidance exists. |
| Afatinib PRE EGFR TKI | No initial renal dose reduction for mild-moderate impairment; for severe renal impairment (eGFR ~15-29) a reduced starting dose (30 mg daily) is advised per labeling, with titration as tolerated. The practical priority is holding/reducing for grade >=2-3 diarrhea to prevent prerenal AKI. | Yes Not appreciably dialyzable—highly protein-bound (~95%), lipophilic, with predominantly fecal/biliary excretion and minimal renal clearance; hemodialysis is not expected to remove meaningful amounts. |
| Alectinib PSEUDO ALK TKI | No starting-dose change for mild-to-moderate renal impairment; data in severe impairment/ESKD are limited (alectinib is hepatically metabolized with <1% renal excretion), so no PK-based renal adjustment is mandated. Hepatic impairment requires dose reduction. | No Highly protein-bound (>99%) and hepatically cleared; not dialyzable and no supplemental dosing expected in ESKD. |
| Alpelisib PRE PI3Kα inhibitor | No dose adjustment for mild-moderate renal impairment; not studied in severe impairment (CrCl <30) or ESKD. Dose modification is driven by hyperglycemia and rash, not by baseline GFR. | Yes Highly protein-bound small molecule; not expected to be meaningfully dialyzable and no ESKD dosing established. |
| Altretamine (hexamethylmelamine) ATN Alkylating agent (methylmelamine) | No established renal-specific dosing algorithm; altretamine is extensively hepatically metabolized with low urinary excretion of unchanged drug. Dose reductions and interruptions are primarily for GI, neurologic and hematologic toxicity. | Yes Not characterized as dialyzable; high lipid solubility, extensive hepatic metabolism and tissue distribution make significant dialytic removal unlikely. Dialysis is not used for drug clearance. |
| Amivantamab AIN EGFR-MET bispecific antibody | No established renal dose adjustment (monoclonal antibody, not renally cleared). Manage by electrolyte repletion and infusion-rate modification; hold for suspected AIN rather than dose-reduce. | No Large IgG bispecific antibody — not dialyzable and cleared by reticuloendothelial proteolysis; no ESKD dose change expected. Electrolyte management is the renal priority in advanced CKD. |
| Amsacrine LYTE Topoisomerase II inhibitor (acridine) | Pharmacokinetic data support initial dose reduction (on the order of 30-40%) in patients with severe hepatic or renal impairment or with documented impaired drug clearance, since elimination is predominantly hepatobiliary and is prolonged in organ dysfunction. | — Unlikely to be efficiently dialyzed given very high plasma protein binding (~96-98%) and hepatobiliary elimination; dialysis is reserved for managing TLS metabolic complications rather than drug removal. |
| Arsenic trioxide PRE Differentiating agent | No formal CrCl-based dose schedule is established, but because arsenic is largely renally excreted, dose reduction and intensified monitoring are advised in significant renal impairment; the label notes caution and reduced clearance in renal dysfunction. Standard induction is 0.15 mg/kg/day. | Yes Arsenic is partially dialyzable, and case experience supports continuing ATO with dosing around hemodialysis sessions in ESKD; given renal excretion, careful exposure/QT monitoring is essential. This contrasts with most agents in this batch. |
| Asciminib HTN BCR-ABL STAMP inhibitor | No dose adjustment required for renal impairment in labeling (renal clearance is minor); use general caution in advanced CKD. Hepatic metabolism predominates. | Yes Highly protein-bound; not expected to be dialyzable. No specific ESKD dosing required given minimal renal clearance. |
| Asparaginase PRE Enzyme | Large protein cleared by reticuloendothelial proteolysis, not renal filtration - no renal dose adjustment. Management is toxicity-driven (hold/switch for pancreatitis, severe hypersensitivity, or thrombosis). | No Large enzyme; not dialyzable. Dialysis/CRRT is used to support AKI or refractory hyperammonemia, not to clear the drug. |
| Atezolizumab AIN Anti-PD-L1 antibody | No baseline renal dose adjustment (fixed-dose antibody not renally cleared). The relevant 'adjustment' is immune-toxicity grading: per consensus guidance, withhold for grade 2 (creatinine 2-3x baseline) and treat with steroids, and permanently discontinue for grade 3-4 or recurrent severe nephritis. | No Not dialyzable—an IgG1 monoclonal antibody cleared by reticuloendothelial catabolism; not removed by hemodialysis and no dose supplementation needed. ESKD patients can receive standard dosing. |
| Avapritinib PRE KIT / PDGFRA inhibitor | No dose adjustment for mild-moderate renal impairment; severe impairment/ESKD not well studied (hepatic CYP3A4 metabolism). Modifications driven by edema, CNS effects and cytopenias. | Yes Highly protein-bound; not expected to be dialyzable. No established ESKD dosing. |
| Avelumab AIN Anti-PD-L1 antibody | No baseline renal dose adjustment (fixed-dose antibody, not renally cleared). Toxicity-based modification follows irAE grading: withhold for grade 2 nephritis with steroids; permanently discontinue for grade 3-4 or recurrent severe nephritis. Avelumab requires premedication to prevent infusion reactions (unrelated to renal dosing). | No Not dialyzable—IgG1 monoclonal antibody cleared by reticuloendothelial catabolism; not removed by hemodialysis, no supplemental dosing, standard dosing in ESKD. |
| Azacitidine ATN Hypomethylating agent | No starting-dose adjustment is required for baseline renal impairment, but the label mandates a 50% dose reduction of the next cycle if unexplained serum bicarbonate <20 mEq/L or a rise in BUN/creatinine occurs, with resumption only after recovery to baseline. Use with caution and closer monitoring in CKD. | — Azacitidine and its metabolites are partly renally cleared; specific hemodialysis removal data are limited. It is given to dialysis patients in practice with careful monitoring, but no validated supplemental dosing exists. |
| Belantamab mafodotin PRE Antibody-drug conjugate (BCMA/MMAF) | No renal dose adjustment defined; pharmacokinetics are not expected to depend on renal clearance for an IgG-MMAF conjugate. Dosing modifications are driven by ocular findings, not renal function. | No Not dialyzable (large ADC; non-cleavable linker, internalization-dependent MMAF). No supplemental dosing for HD/PD. |
| Belzutifan PRE HIF-2α inhibitor | No dose adjustment for mild-to-moderate renal impairment; severe impairment (eGFR <30) and ESKD are not well studied. Standard 120 mg once daily; modifications are driven by anemia and hypoxia rather than CrCl. | Yes Not characterized; belzutifan is highly protein-bound and primarily metabolized by UGT2B17/CYP2C19, so it is unlikely to be substantially removed by dialysis. No ESKD dosing guidance exists. |
| Bendamustine PRE Alkylator | Use with caution and consider dose reduction for CrCl <40 mL/min; not recommended in severe renal impairment per labeling owing to limited data. Active metabolites contribute little to overall effect, but exposure data in advanced CKD are sparse - individualize with pharmacy. | Yes Parent drug is rapidly hydrolyzed/metabolized with short half-life, so it is not meaningfully dialyzable; reported ESKD/HD cases dosed bendamustine successfully with careful timing rather than relying on dialytic removal. |
| Bicalutamide AIN Nonsteroidal antiandrogen | No dose adjustment for renal impairment. Dose with caution in severe hepatic impairment (slower (R)-enantiomer elimination). | Yes Not meaningfully dialyzable expected given high protein binding and hepatic clearance; not clinically relevant to dosing. |
| Binimetinib PRE MEK inhibitor | No dedicated renal dose adjustment; no change recommended for mild-moderate impairment, and severe impairment/dialysis are not studied. Modifications are driven by CK, LVEF, retinopathy, and hepatic toxicity. | — Highly protein-bound oral small molecule; not expected to be appreciably dialyzed. No validated ESKD dosing. |
| Bleomycin ATN Antitumor antibiotic | Reduce dose in renal impairment; common guidance reduces by ~25% for CrCl 40-50 mL/min and progressively more (up to ~50-60%) for CrCl 10-40 mL/min, reflecting the exponential rise in half-life below ~25-35 mL/min. Verify against local protocol. | — Low-molecular-weight and water-soluble; case-level data suggest some removal by dialysis, but it is not relied upon clinically. Dosing in dialysis patients should be conservative and individualized. |
| Blinatumomab PRE BiTE (CD19×CD3) | No specific renal dose adjustment for CrCl >=30 mL/min; pharmacokinetic data in severe impairment (CrCl <30) and dialysis are limited, so use with monitoring. The practical levers are step-up dosing and interruption for severe CRS/TLS rather than renal dose modification of the continuous infusion. | No Not dialyzable as a therapeutic—a ~54 kDa bispecific protein given by continuous infusion with a very short half-life (~2 hours), cleared by catabolism; renal replacement therapy is used to treat TLS/AKI, not to remove the drug, and no supplemental dosing is needed. |
| Bortezomib TMA Proteasome inhibitor | No renal dose adjustment required at any level of renal function, including dialysis (bortezomib is hepatically metabolized via CYP-mediated deboronation). This renal-sparing profile is a key reason it anchors regimens for myeloma with kidney involvement. | — Not appreciably dialyzed; on dialysis days, administer after the HD session per label. No supplemental dose required. |
| Bosutinib PSEUDO BCR-ABL TKI | Per labeling, reduce the starting dose in baseline renal impairment: CrCl 30-50 mL/min use a reduced starting dose (e.g., 400 mg in the resistant/intolerant setting), and CrCl <30 mL/min use a further-reduced dose (e.g., 300 mg). Titrate per response and tolerability. | — Highly protein-bound and hepatically metabolized; not expected to be appreciably dialyzed and no supplemental post-dialysis dosing is established. Use clinical judgment in ESKD. |
| Brentuximab vedotin PRE Antibody-drug conjugate (CD30/MMAE) | Per label, severe renal impairment (CrCl <30) increases MMAE exposure and adverse events - use with caution and avoid where alternatives exist; no adjustment needed for mild-moderate impairment. MMAE is a CYP3A4 substrate. | — Not appreciably dialyzed (large ADC; protein-bound MMAE). No supplemental dosing guidance for HD/PD. |
| Brigatinib PSEUDO ALK TKI | Reduce the dose for severe renal impairment (eGFR <30 mL/min/1.73 m2) - e.g., decrease the maintenance dose by ~50% per labeling. No adjustment is needed for mild-to-moderate impairment. Hepatic impairment also warrants reduction. | — Highly protein-bound (~91%) and hepatically metabolized; not expected to be meaningfully dialyzed. ESKD data are limited - monitor clinically. |
| Busulfan TMA Alkylator | Busulfan clearance is largely hepatic (GST-mediated); no formal renal CrCl dose banding, but AUC-targeted (therapeutic-drug-monitoring) dosing is standard to avoid the high exposures linked to TMA and VOD. Reduced clearance at high doses warrants level monitoring. | No Busulfan is moderately dialyzable in principle, but TDM-guided dosing (not dialysis) is the control strategy; dialysis is reserved for managing TA-TMA-related renal failure rather than for drug removal. |
| Cabazitaxel PRE Taxane | Hepatically (CYP3A) metabolized with minimal renal excretion - no formal renal dose adjustment for mild-moderate impairment; use caution in severe impairment/ESKD given limited data. Reduce dose for hepatic impairment and with strong CYP3A inhibitors. | No Highly protein-bound and non-renally cleared; not dialyzable. No HD-timed dosing established. |
| Cabozantinib HTN VEGFR/MET TKI | No dose adjustment for mild-to-moderate renal impairment; cabozantinib has not been studied in severe renal impairment or ESKD, so use is cautious there. It is hepatically metabolized (CYP3A4), and dose reduction is recommended for hepatic impairment. | Yes Highly protein-bound (~99.7%) and hepatically cleared, so it is not meaningfully dialyzable; no supplemental dosing rationale for HD, and data in dialysis patients are sparse. |
| Capecitabine PRE Pyrimidine analog (oral 5-FU) | Per labeling/PK data: no adjustment for mild impairment (CrCl 51-80); reduce to 75% of starting dose for moderate impairment (CrCl 30-50); contraindicated for severe impairment (CrCl <30), where all patients experienced grade 3-4 toxicity. | — Capecitabine and 5-FU have short half-lives and are not managed by dialysis; the renally cleared catabolites (e.g., fluoro-beta-alanine) accumulate in renal failure, which is why severe impairment is contraindicated rather than dialysis-supported. |
| Capivasertib PRE AKT inhibitor | No dedicated renal dose adjustment for mild–moderate impairment; severe impairment/ESKD not well studied. Dose modification is driven by GI/metabolic toxicity grade. Capivasertib is given on an intermittent (4-days-on/3-days-off) schedule. | — Hepatically metabolized small molecule (CYP3A4); dialyzability not well characterized and unlikely to be the management lever. In advanced CKD, focus on volume/glucose management. |
| Capmatinib PSEUDO MET inhibitor | No starting-dose adjustment for mild-moderate renal impairment; severe impairment and dialysis are not well studied (use with caution). Dose modifications are driven by edema, ILD/pneumonitis, and hepatotoxicity rather than a CrCl rule. | — Highly protein-bound oral small molecule; not expected to be appreciably dialyzed. No validated ESKD dosing. |
| Carfilzomib TMA Proteasome inhibitor | Per label no starting-dose adjustment is required across renal function including dialysis (carfilzomib is rapidly metabolized by peptidase/epoxide hydrolase, not renally cleared); however, given the high rate of renal events, monitor closely and hold for TMA/AKI rather than adjusting prophylactically. | Yes On hemodialysis days, administer carfilzomib after the HD session (per label) because of theoretical dialytic clearance considerations; the parent drug is largely cleared by non-renal metabolism. Dialysis is otherwise used to support TMA/AKI. |
| Carmofur (HCFU) TMA Antimetabolite (oral 5-FU prodrug) | No validated renal nomogram; use caution and consider reduction in significant renal impairment given renal elimination of 5-FU metabolites, per regional labeling. | — Not well characterized; dialysis is supportive for AKI rather than for drug removal. |
| Carmustine (BCNU) CIN Nitrosourea alkylator | No precise CrCl-banded schema; reduce or avoid in baseline renal impairment and cap cumulative lifetime dose. Hold subsequent courses for a sustained creatinine rise rather than waiting for symptomatic CKD. | Yes Highly lipophilic, rapidly metabolized parent drug; not meaningfully removed by dialysis and dialysis is not a management strategy. ESKD use is essentially limited to individualized conditioning protocols. |
| Casdatifan PRE HIF-2α inhibitor (investigational) | Not established (investigational). HIF-2α inhibitors are hepatically metabolized; meaningful renal-clearance dependence is not expected, but formal renal-impairment dosing has not been published. Many ccRCC patients have reduced nephron mass after nephrectomy, which is relevant to baseline GFR interpretation. | — Not characterized; a protein-bound, hepatically cleared small molecule is unlikely to be appreciably dialyzed. No ESKD dosing data. |
| Catumaxomab PRE Trifunctional bispecific (EpCAM×CD3) | No renal dose adjustment defined; the agent is given intraperitoneally as an antibody and is not renally cleared. The actionable interventions are hemodynamic/supportive rather than renal dosing. | No A large trifunctional antibody — not dialyzable and cleared by proteolysis; no ESKD dosing guidance. Renal management is volume- and electrolyte-focused. |
| Cemiplimab AIN Anti-PD-1 antibody | No baseline renal dose adjustment (fixed-dose antibody, not renally cleared). Toxicity-based modification follows irAE grading: withhold for grade 2 nephritis with steroids; permanently discontinue for grade 3-4 or recurrent severe nephritis. | No Not dialyzable—IgG4 monoclonal antibody cleared by reticuloendothelial catabolism; not removed by hemodialysis, no supplemental dosing, standard dosing in ESKD. |
| Ceritinib PSEUDO ALK TKI | No starting-dose change for mild-to-moderate renal impairment (negligible renal excretion); severe-impairment/ESKD data are limited, so use clinical monitoring. The practical 'renal' adjustment is interruption/reduction when GI toxicity threatens volume status. Hepatic impairment requires dose reduction. | — Highly protein-bound (~97%) and hepatically metabolized; not expected to be dialyzed and no supplemental dosing established. |
| Chlorambucil SIADH Alkylating agent (nitrogen mustard) | No formal renal dose-adjustment scheme is established; chlorambucil is extensively hepatically metabolized to phenylacetic acid mustard with limited unchanged renal excretion. Dosing is guided mainly by hematologic tolerance. | Yes Not characterized as dialyzable and unlikely to be efficiently removed given rapid metabolism and protein binding; dialysis is not used for drug clearance. |
| Ciltacabtagene autoleucel PRE BCMA CAR-T cell therapy | A fixed cell product with no renal dose adjustment; renal dosing applies to the lymphodepleting fludarabine. | — Not applicable (a living-cell product). Dialysis supports AKI/tumor lysis rather than removing the therapy. |
| Cladribine PRE Purine analog | Substantially renally eliminated; the label advises caution and consideration of dose reduction with close monitoring in renal impairment. No firmly validated CrCl bands exist; published practice uses reduced/spaced (e.g. every-other-week) dosing in severe CKD, where complete remission is still achievable. | Yes Not reliably characterized and not considered readily dialyzable for drug removal; dialysis is used to manage tumor-lysis metabolic derangements. |
| Clofarabine PRE Purine analog | Limited renal pharmacokinetic data; the label advises starting at a reduced dose and monitoring closely when CrCl is 30-60 mL/min, and clofarabine is not recommended (avoid) when CrCl is below 30 mL/min. Renal clearance accounts for a substantial fraction of elimination, so impaired clearance raises systemic exposure. | — Not formally characterized; no established supplemental dosing for hemodialysis. Given its small size and renal elimination there is theoretical removal, but it is not used in dialysis-dependent patients and HD is employed only to manage AKI complications, not to dose the drug. |
| Cobimetinib ATN MEK inhibitor | No renal dose adjustment recommended for mild-moderate impairment; severe impairment and dialysis are not studied. Dose modification is driven mainly by CK elevation, retinopathy, LVEF, and photosensitivity. | — Highly protein-bound oral small molecule; not expected to be meaningfully dialyzed. No validated ESKD dosing. |
| Copanlisib HTN Pan-PI3K inhibitor | No specific dose adjustment for renal impairment in labeling; hepatic metabolism predominates. Dose modification is driven by hypertension, hyperglycemia and cytopenias rather than GFR. | Yes Protein-bound IV agent given intermittently; not expected to be dialyzable, and ESKD dosing is not established. |
| Crizotinib RCYST ALK/ROS1/MET TKI | No starting-dose change for mild-to-moderate renal impairment (CrCl >=30). For severe renal impairment not on dialysis (CrCl <30), reduce the dose (e.g., to 250 mg once daily) per labeling. Hepatic impairment also requires adjustment. | — Highly protein-bound (~91%) and hepatically metabolized; not appreciably dialyzed. ESKD dosing data are limited - use clinical monitoring. |
| Cytarabine PRE Nucleoside analog | Standard-dose cytarabine needs little renal adjustment; for HIGH-dose cytarabine, reduced renal function (and age) increase the risk of neurotoxicity (cerebellar) so dose reduction is advised when creatinine/CrCl worsens. Renal handling is a high-dose neurotoxicity concern more than a nephrotoxicity one. | — Cytarabine is rapidly deaminated to inactive ara-U with a short half-life; it is not primarily managed by dialysis, though dialysis is used to treat TLS-related renal failure and electrolyte derangements. |
| Dacarbazine PRE Alkylator | No established renal CrCl dose modification; dacarbazine is partly renally excreted but dose adjustment is driven mainly by hematologic toxicity and hepatic function. Use general caution and maintain hydration in renal impairment. | — Short-lived parent prodrug undergoing hepatic activation; not a drug managed by dialysis. ESKD data are minimal. |
| Dactinomycin (actinomycin D) LYTE Antitumor antibiotic | No well-established renal dose-adjustment scheme; dactinomycin is largely excreted in bile/feces with minor renal elimination. Dose modification is generally driven by hepatic toxicity and myelosuppression rather than kidney function. | Yes Not meaningfully dialyzable; high tissue binding and predominantly biliary/fecal elimination. Dialysis has a role only for managing TLS-related metabolic derangements, not for drug removal. |
| Daratumumab PRE Anti-CD38 antibody | No renal dose adjustment; antibody clearance is target-mediated/reticuloendothelial, not renal. Standard IV or subcutaneous dosing is used regardless of CrCl, including in dialysis-dependent patients per trial and case data. | No Not dialyzed — a large IgG1 antibody not removed by HD/PD; full standard dosing in ESKD. Renal recovery off dialysis has been reported with daratumumab-based therapy. |
| Darolutamide LYTE Androgen receptor inhibitor (ARSI) | Per pharmacokinetic data and labeling, a reduced starting dose (e.g., 300 mg twice daily) should be considered in severe renal impairment (and in moderate hepatic impairment) because systemic exposure is increased; standard 600 mg twice daily otherwise. | — Dialyzability not formally established; darolutamide is substantially protein-bound and hepatically metabolized, so dialysis is unlikely to be a primary management consideration. Use clinical judgment and labeling in dialysis patients. |
| Dasatinib GLOM BCR-ABL TKI | No formal renal dose adjustment is specified (dasatinib is extensively hepatically metabolized with <4% renal excretion); however, the practical 'renal' adjustment is dose reduction or drug switch when treatment-emergent proteinuria appears. | — Dasatinib is highly protein-bound and extensively metabolized; it is not appreciably dialyzed and needs no supplemental post-dialysis dose. Standard dosing applies in ESKD with clinical monitoring. |
| Datopotamab deruxtecan (Dato-DXd) ATN Antibody-drug conjugate (TROP2/DXd) | No dedicated renal dose adjustment established; not studied in severe renal impairment/ESKD. Modify dose/hold for toxicity per label. The antibody component is not renally cleared; small-molecule payload exposure in advanced CKD is not well defined. | No The IgG–ADC is not dialyzable; the released small-molecule DXd payload's dialyzability is not characterized. No ESKD dosing guidance — use clinical judgment and close monitoring. |
| Decitabine PRE Hypomethylating agent | No formal renal dose adjustment is established in the label; decitabine is largely metabolized by deamination (cytidine deaminase) rather than renal excretion. Use caution in significant renal impairment given limited data and monitor renal function closely. | — Not well characterized; the short plasma half-life and rapid deamination limit the rationale for dialytic dosing. Hemodialysis is used to treat AKI/metabolic complications, not to adjust drug levels. |
| Denileukin diftitox PRE Immunotoxin (IL-2–diphtheria) | Weight-based dosing (9 micrograms/kg/day for 5 days every 21 days); modification is driven by toxicity (albumin, organ function), not by CrCl. No CrCl-based dose thresholds are defined. | — Not established — a large fusion protein; AKI here is managed hemodynamically rather than by dialytic drug removal. |
| Denosumab LYTE Anti-RANKL antibody | No dose reduction for renal function (cleared by the reticuloendothelial system, independent of GFR), but in CKD stage 4-5/dialysis the hazard is hypocalcemia - intensify calcium/vitamin D and monitoring rather than altering the dose. Avoid concurrent same-indication dosing of Xgeva and Prolia. | No Monoclonal antibody (IgG2); not dialyzable and pharmacokinetics are unaffected by dialysis. Hemodialysis is used to manage the metabolic consequences, not to remove the drug. |
| Dinutuximab PRE Anti-GD2 antibody | No specific renal dose adjustment in labeling (a monoclonal antibody); manage infusion rate and interruptions for capillary leak, pain and hemodynamic instability. | No A monoclonal antibody; not dialyzable. ESKD dosing is not established (used in pediatric neuroblastoma). |
| Docetaxel PRE Taxane | Hepatically (CYP3A4) metabolized and biliary excreted - no renal dose adjustment; reduce dose (or avoid) with significant hepatic dysfunction/elevated bilirubin and transaminases, which raise toxicity risk. | No Highly protein-bound, large volume of distribution, non-renally cleared; not dialyzable. Tolerated in dialysis and transplant patients with standard dosing and supportive care. |
| Dostarlimab AIN Anti-PD-1 antibody | No baseline renal dose adjustment (fixed-dose antibody, not renally cleared). Toxicity-based modification follows irAE grading: withhold for grade 2 nephritis with steroids; permanently discontinue for grade 3-4 or recurrent severe nephritis. | No Not dialyzable—IgG4 monoclonal antibody cleared by reticuloendothelial catabolism; not removed by hemodialysis, no supplemental dosing, standard dosing in ESKD. |
| Doxifluridine TMA Antimetabolite (oral 5-FU prodrug) | No validated renal nomogram. Given a documented renal clearance component for doxifluridine and renal elimination of 5-FU metabolites, consider caution/dose reduction in significant renal impairment per regional labeling. | — Not well characterized; dialysis is supportive for AKI rather than established for drug removal. |
| Doxorubicin GLOM Anthracycline | No renal dose adjustment is required — doxorubicin is hepatically metabolized and biliary-excreted, so dosing is guided by hepatic function and bilirubin rather than renal function. Renal impairment does not mandate dose reduction. | No Not dialyzable to any clinically meaningful extent; doxorubicin is large, highly protein- and tissue-bound, with a very large volume of distribution, so hemodialysis does not remove it and no supplemental dosing is needed in ESKD. |
| Durvalumab AIN Anti-PD-L1 antibody | No baseline renal dose adjustment (fixed-dose antibody, not renally cleared). Toxicity-based modification follows irAE grading: withhold for grade 2 nephritis with steroids; permanently discontinue for grade 3-4 or recurrent severe nephritis. | No Not dialyzable—IgG1 monoclonal antibody cleared by reticuloendothelial catabolism; not removed by hemodialysis, no supplemental dosing, standard dosing in ESKD. |
| Duvelisib PRE PI3Kδ/γ inhibitor | No renal dose adjustment specified (hepatic CYP3A4 metabolism); use caution in CKD. Dose modifications are driven by colitis, hepatotoxicity, infection and cytopenias. | Yes Highly protein-bound; not expected to be dialyzable. No ESKD dosing established. |
| Elacestrant PRE Oral selective estrogen-receptor degrader (SERD) | No renal dose adjustment is established for mild–moderate impairment; severe impairment/ESKD are not well studied. Dose reductions per label are driven by hepatic impairment and CYP3A4 interactions, not renal function. | Yes Highly protein-bound and hepatically metabolized; not expected to be dialyzable. No ESKD dosing guidance exists. |
| Elotuzumab LYTE Anti-SLAMF7 mAb | No dose adjustment for any degree of renal impairment, including severe impairment and end-stage renal disease on dialysis (Berdeja 2015). The actionable renal adjustment is to the partner immunomodulator, not to elotuzumab. | No A ~150 kDa IgG1 antibody — not removed by hemodialysis and cleared by proteolysis; pharmacokinetics are unchanged in dialysis patients, so no peri-dialysis timing change is needed. |
| Elranatamab PRE Bispecific (BCMA×CD3) | No specific renal dose adjustment is established; elranatamab pharmacokinetics are not meaningfully renally dependent. Two-step priming dosing and holds for severe CRS, plus TLS prophylaxis, are the operative levers rather than renal dose modification. | No Not dialyzable—an IgG-based bispecific antibody cleared by catabolism; not removed by hemodialysis and no supplemental dosing needed. Renal replacement therapy treats AKI/TLS, not drug clearance. |
| Enasidenib PRE IDH2 inhibitor | No dedicated renal dose adjustment is established; enasidenib was not studied in severe renal impairment/ESKD. Standard dose is 100 mg orally once daily, modified for toxicity (including differentiation syndrome and indirect hyperbilirubinemia), not for CrCl. | Yes Not characterized; enasidenib is highly protein-bound and hepatically metabolized, so it is not expected to be appreciably removed by hemodialysis. No HD-specific dosing guidance exists. |
| Encorafenib ATN BRAF inhibitor | No dedicated renal dose adjustment established; no change recommended for mild-moderate impairment, and severe impairment/dialysis are not studied (use with caution). Dose modifications are driven mainly by CK, hepatic, and cardiac (QT) toxicity. | Yes Highly protein-bound oral small molecule; not expected to be appreciably removed by dialysis. No validated ESKD dosing. |
| Enfortumab vedotin ATN Antibody-drug conjugate (Nectin-4/MMAE) | No starting-dose adjustment for mild-moderate renal impairment; per label, the recommended dose has been administered to patients with CrCl >=15 mL/min, and the drug is used in real-world practice at eGFR <30. Limited data in ESKD/dialysis. The cytotoxic exposure is the released MMAE (hepatically metabolized via CYP3A4), not renally cleared parent ADC. | — The intact ADC and protein-bound MMAE are not meaningfully dialyzed; HD is used to support AKI/metabolic complications, not to remove the drug. Terminal half-life ~3.4 days guides how long toxicity (e.g., refractory hyperglycemia) may persist. |
| Entrectinib PSEUDO TRK/ROS1 TKI | No renal dose adjustment for mild-to-moderate impairment; entrectinib is hepatically (CYP3A4) metabolized with low renal clearance. The creatinine rise should not be misread as AKI requiring dose reduction. Limited data in severe impairment/dialysis. | — Not characterized; highly protein-bound, lipophilic, non-renally cleared — unlikely to be appreciably dialyzed. No ESKD dosing guidance. |
| Enzalutamide HTN Androgen-receptor inhibitor | No dose adjustment for mild–moderate renal impairment; severe impairment and ESKD have not been formally studied. Reduce dose in concomitant strong CYP2C8 inhibitors and for hepatic impairment per label. | Yes Highly protein-bound and hepatically metabolized; not expected to be dialyzable. No established ESKD dosing — use clinical judgment and blood-pressure-directed care. |
| Epcoritamab PRE Bispecific (CD20×CD3) | No specific renal dose adjustment defined; IgG bispecific exposure is not expected to depend on renal clearance. No dedicated data in severe impairment/ESKD. | No Not dialyzable (large IgG, reticuloendothelial catabolism). No supplemental dosing for HD/PD. |
| Erdafitinib LYTE FGFR inhibitor | No starting-dose change for mild-moderate renal impairment; severe impairment and dialysis are not well studied (use with caution). The principal 'dose adjustment' is phosphate-guided titration/interruption rather than a CrCl-based rule. | — Highly protein-bound oral small molecule; not expected to be appreciably dialyzed. No validated ESKD dosing — phosphate handling is also altered in ESKD, complicating the pharmacodynamic phosphate biomarker. |
| Eribulin PRE Microtubule inhibitor | Reduce dose to 1.1 mg/m2 for CrCl 30-50 mL/min (moderate impairment); PK data support this matching exposure seen at 1.4 mg/m2 with normal function. Limited data below CrCl 30 mL/min - use caution. | Yes Highly protein-bound with a large volume of distribution and predominantly hepatobiliary elimination; not expected to be dialyzable. No HD-timed dosing established. |
| Erlotinib GLOM EGFR TKI | No specific dose reduction is established for renal impairment (erlotinib is hepatically metabolized via CYP3A4/1A2 and biliary-excreted); use caution in severe impairment as renal data are sparse, and manage GI-driven volume depletion proactively. The pancreatic-cancer regimen pairs it with gemcitabine, which has its own renal considerations. | Yes Not appreciably dialyzable—highly protein-bound (~93%), lipophilic, with predominantly hepatic clearance and minimal renal elimination; hemodialysis is not expected to remove meaningful drug. |
| Estramustine PRE Hormonal–alkylating conjugate | No established CrCl-based dose algorithm; use caution with cardiovascular/cerebrovascular disease and in heart failure. It is contraindicated with active thromboembolic disorders. | — Not characterized/not relevant (highly protein-bound and lipophilic). |
| Etoposide PRE Topoisomerase II inhibitor | Reduce dose for renal impairment: roughly 75% of dose for CrCl 15-50 mL/min and consider further reduction below 15 mL/min, because renal clearance contributes meaningfully and hypoalbuminemia raises free drug. | Yes Highly protein-bound (~95%); only modestly removed by hemodialysis. Dialysis is used for TLS-related metabolic complications, not to clear etoposide; give dose after HD on dialysis days if used. |
| Fludarabine PRE Purine analog | Per PK/labeling: reduce dose for CrCl 30-70 mL/min (commonly ~20% reduction) and avoid for CrCl <30 mL/min. Prospective dose-adjustment studies show CrCl-banded dosing yields equivalent exposure and acceptable safety; full dosing in unrecognized impairment risks severe (even fatal neuro-) toxicity. | — 2-F-ara-A is renally cleared, so ESKD markedly prolongs exposure; data on dialytic removal are limited and fludarabine is generally avoided (rather than dialysis-supported) in severe impairment. In conditioning protocols, PK-guided/reduced dosing is used. |
| Fotemustine CIN Nitrosourea (alkylating) | Use caution and consider dose reduction or avoidance in significant renal impairment; specific renal dosing thresholds are not well established for fotemustine. Withhold for evolving renal dysfunction and reassess cumulative exposure. | — Dialyzability is not well characterized; nitrosoureas are lipophilic and rapidly metabolized, so dialysis is not a relied-upon removal strategy. Manage by dose limitation and monitoring rather than dialysis timing. |
| Fruquintinib HTN VEGFR TKI | No specific renal dose adjustment for mild–moderate impairment; not adequately studied in severe renal impairment/ESKD. Modify dose for grade of hypertension/proteinuria per label rather than for GFR alone. | — Highly protein-bound small molecule with hepatic metabolism; not expected to be appreciably dialyzed. No established ESKD dosing — monitor blood pressure and proteinuria closely. |
| Futibatinib LYTE FGFR inhibitor | No starting-dose change for mild-moderate renal impairment; severe impairment/dialysis not well studied. Phosphate-guided modification, not a CrCl rule, governs dosing. | — Highly protein-bound oral small molecule; not expected to be appreciably dialyzed. No validated ESKD dosing; phosphate-based PD monitoring is confounded in ESKD. |
| Gefitinib GLOM EGFR TKI | No defined renal dose adjustment (hepatic CYP3A4 metabolism, biliary excretion; <4% renal elimination); caution in severe impairment given limited data. The intervention for glomerular toxicity is drug discontinuation, not dose titration. | Yes Not appreciably dialyzable—highly protein-bound (~90%), lipophilic, large volume of distribution with predominantly hepatic clearance; hemodialysis is not expected to remove meaningful amounts. |
| Gemtuzumab ozogamicin PRE Antibody-drug conjugate (CD33/calicheamicin) | No specific renal dose adjustment; dose decisions are driven by hepatic function and VOD risk, not renal clearance. Calicheamicin is hepatically handled. | — Not appreciably dialyzed (large ADC; protein-bound calicheamicin). HD/CRRT in VOD is for fluid/AKI support, not drug removal. |
| Gilteritinib PRE FLT3 inhibitor | No dose adjustment for mild-moderate renal impairment; severe impairment/ESKD not well studied (predominantly hepatic CYP3A4 metabolism). Manage interruptions for differentiation syndrome/TLS/PRES rather than by GFR. | Yes Highly protein-bound; not appreciably dialyzable. Dialysis is used for TLS metabolic complications, not drug removal. |
| Glasdegib PRE Hedgehog (SMO) inhibitor | No dose adjustment recommended for mild-moderate renal impairment; safety/PK in severe renal impairment were not established at approval (labeled limitation; post-marketing study required). Hepatic CYP3A4 metabolism predominates. | Yes Highly protein-bound small molecule; not expected to be appreciably dialyzable, and ESKD dosing is not established. |
| Glofitamab PRE Bispecific (CD20×CD3) | No specific renal dose adjustment defined; IgG bispecific exposure is not expected to be renally dependent. No dedicated data in severe impairment/ESKD. | No Not dialyzable (large IgG, reticuloendothelial clearance). No supplemental dosing for HD/PD. |
| Hydroxyurea PRE Ribonucleotide reductase inhibitor | Hydroxyurea is predominantly renally excreted. The label and pharmacokinetic data support reducing the starting dose in renal impairment (commonly halving the dose when CrCl < 60 mL/min and using marked reductions or avoidance in ESKD) to prevent excessive myelosuppression; titrate to blood counts. | Yes Yes — hydroxyurea is a small (76 Da), water-soluble molecule that is readily removed by hemodialysis. In dialysis-dependent patients, dosing is commonly given after the HD session and reduced; counts must be followed closely. |
| Ibandronate ATN Bisphosphonate | Oral/IV for osteoporosis: no adjustment for CrCl ≥30 mL/min; not recommended (or use with caution) below 30 mL/min. Oncology IV dosing should be reduced and infused slowly in renal impairment; withhold for acute decline in renal function and reassess. | — Negligible plasma drug at steady state due to rapid bone uptake; not meaningfully dialyzed. In hemodialysis patients a reduced IV dose (e.g., 2 mg) given after dialysis achieves equivalent bone binding (Bergner 2005). |
| Ibritumomab tiuxetan PRE Radioimmunotherapy (Y-90 anti-CD20) | Administered activity is capped by platelet count (e.g. reduced to 0.3 mCi/kg if platelets 100,000-149,000/uL; contraindicated if platelets <100,000/uL or >25% lymphomatous marrow involvement) — a hematologic threshold. No renal CrCl-based dose adjustment is defined; the kidney does not drive dosing. | No The radioimmunoconjugate is not dialyzable. Dialysis is relevant only for managing TLS metabolic derangements, not for removing the drug. |
| Ibrutinib HTN BTK inhibitor | No dose adjustment for mild-to-moderate renal impairment (CrCl ≥30 mL/min); severe impairment (CrCl <30) and dialysis are not well studied — use with caution. Ibrutinib is hepatically (CYP3A) cleared, so hepatic impairment, not renal, drives dose reduction; <10% renal excretion of metabolites. | No Not dialyzable in any meaningful sense — highly protein-bound (~97%) small molecule with hepatic clearance. No supplemental dosing after HD is needed. |
| Idarubicin PRE Anthracycline | Primarily hepatobiliary elimination; reduce in hepatic dysfunction. The manufacturer advises caution/consideration of reduction in renal impairment (e.g. serum creatinine >2 mg/dL) but provides no precise CrCl algorithm; cumulative anthracycline cardiotoxicity limits dosing. | Yes Not appreciably dialyzable (large volume of distribution and tissue binding); dialysis manages tumor-lysis derangements. |
| Idecabtagene vicleucel PRE BCMA CAR-T cell therapy | No CAR-T dose adjustment for renal function (it is a fixed cell product); the renal-relevant lever is the conditioning regimen, where fludarabine requires renal dose consideration. Cohort data show CAR-T is feasible even with reduced renal function or on dialysis. | — Not applicable — a living-cell product. Dialysis is used to support AKI/tumor lysis, not to remove the therapy. |
| Idelalisib PRE PI3Kδ inhibitor | No specific renal dose adjustment is defined; metabolism is hepatic (CYP3A/aldehyde oxidase). Caution and monitor in CKD; dose changes are driven by colitis, hepatotoxicity and cytopenias. | Yes Extensively protein-bound; not meaningfully dialyzable. No established ESKD dosing. |
| Imatinib LYTE BCR-ABL TKI | Reduce the starting dose by ~50% for severe renal impairment (CrCl <20 mL/min) and use caution with moderate impairment; standard starting doses are otherwise unchanged. Adjust for tolerability rather than by a strict eGFR algorithm. | Yes Imatinib is highly protein-bound (~95%) with a large volume of distribution and is not appreciably removed by hemodialysis; supplemental post-dialysis dosing is not required. |
| Imetelstat PRE Telomerase inhibitor | No dedicated renal dose adjustment is established in lower-risk MDS labeling. As an oligonucleotide, elimination is largely via nuclease metabolism/tissue distribution rather than glomerular filtration; mild-moderate renal impairment is not expected to require change. No data in severe impairment or dialysis. | Yes Not characterized; large protein-bound oligonucleotides are generally not appreciably removed by hemodialysis. No ESKD dosing guidance. |
| Infigratinib LYTE FGFR inhibitor | Standard 125 mg daily for 21 of 28 days. No dedicated adjustment is established for mild-moderate renal impairment, but reduced GFR raises hyperphosphatemia risk and warrants closer monitoring; severe-impairment data are limited. | Yes Not established; highly protein-bound and CYP3A4-metabolized, so it is not expected to be meaningfully dialyzable. |
| Inotuzumab ozogamicin PRE Antibody-drug conjugate (CD22/calicheamicin) | No specific renal dose adjustment; decisions are driven by hepatic function/VOD risk rather than renal clearance. Calicheamicin is hepatically handled. | — Not appreciably dialyzed (large ADC; protein-bound calicheamicin). HD/CRRT in VOD supports AKI, not drug removal. |
| Irinotecan PRE Topoisomerase I inhibitor | Largely hepatic/biliary elimination, so no formal eGFR-based renal dose table; UGT1A1 poor metabolizers warrant a ~30% starting-dose reduction. Caution and possible reduction in significant hepatic dysfunction (hyperbilirubinemia). | Yes Irinotecan and SN-38 are protein-bound and hepatically/biliary cleared; not effectively removed by dialysis. No HD-timed dosing established. |
| Isatuximab PRE Anti-CD38 antibody | No renal dose adjustment; antibody clearance is target-mediated/reticuloendothelial, not renal. Standard weight-based dosing (10 mg/kg) is used across renal-function strata; ICARIA-MM and IKEMA included patients with renal impairment. | No Not dialyzed — a large IgG1 antibody not removed by HD/PD; standard dosing in ESKD. Dialysis treats TLS complications, not drug levels. |
| Ivosidenib PRE IDH1 inhibitor | No dedicated renal dose adjustment established; no change recommended for mild-moderate impairment, and severe impairment/dialysis are not well studied. Dose interruption is driven by differentiation syndrome, QTc prolongation, and other toxicities rather than a CrCl rule. | — Highly protein-bound oral small molecule; not meaningfully dialyzed. Renal replacement therapy is used to manage AKI/TLS metabolic derangements, not to clear the drug. |
| Ixazomib TMA Proteasome inhibitor | No starting-dose change for mild renal impairment (CrCl >=30). For severe renal impairment (CrCl <30) or ESRD requiring dialysis, reduce the ixazomib dose from 4 mg to 3 mg. Hepatic impairment also requires reduction. | No Ixazomib is not dialyzable to a clinically meaningful degree (highly protein-bound, large volume of distribution); it may be given without regard to dialysis timing. Use the reduced 3 mg dose in dialysis-dependent patients. |
| Lanreotide LYTE Somatostatin analog | Exposure increases with the degree of renal impairment; some labeling recommends a reduced starting dose in moderate-to-severe renal impairment for certain indications. Consult product information for the specific formulation and indication. | Yes Not established as meaningfully dialyzable for supplemental dosing; depot peptide pharmacology and case experience suggest cautious use in hemodialysis without routine post-dialysis supplementation. |
| Larotrectinib PSEUDO TRK inhibitor | No dose adjustment is required for mild/moderate renal impairment (no change to the starting dose). Adults 100 mg PO twice daily; children 100 mg/m2 (max 100 mg) twice daily. Note that moderate-to-severe hepatic impairment does require dose reduction — a useful contrast, since the creatinine bump can be mistaken for a renal-dosing trigger. | Yes Not established; a small-molecule, lipophilic, highly protein-bound drug not expected to be meaningfully dialyzable. |
| Lazertinib SIADH EGFR TKI (3rd-gen) | No established renal dose adjustment (not renally cleared to a significant degree); severe impairment/ESKD not well studied. Manage by sodium/electrolyte correction and drug hold for severe hyponatremia rather than GFR-based dosing. | — Highly protein-bound, hepatically metabolized small molecule; not expected to be appreciably dialyzed. No specific ESKD dosing — focus on sodium and electrolyte management. |
| Lenalidomide ATN Immunomodulatory drug (IMiD) | Per pharmacokinetic data, adjust the starting dose when CrCl <60 mL/min (myeloma labeling): CrCl 30-60 use ~10 mg daily; CrCl <30 not on dialysis use 15 mg every other day; on dialysis use 5 mg once daily, given after dialysis on dialysis days. Disease-specific labels differ; titrate to tolerance. | Yes Yes, lenalidomide is removed by hemodialysis - a 4-hour session cleared ~31% of body drug content. Administer the daily dose after the dialysis session on dialysis days. |
| Lenvatinib HTN VEGFR TKI | Reduce the starting dose for severe renal impairment (CrCl < 30 mL/min) per label (e.g., a lower mg starting dose in thyroid/RCC indications); no adjustment for mild-moderate impairment. Lenvatinib is mainly hepatically metabolized (CYP3A and aldehyde oxidase), so hepatic impairment also drives dose reduction. | Yes Highly protein-bound (~98-99%) and hepatically cleared, so it is not appreciably removed by hemodialysis; dosing in ESKD follows the severe-renal-impairment reduction with toxicity-guided titration. |
| Leuprolide HTN GnRH agonist | No renal dose adjustment; leuprolide is a peptide cleared by peptidase/tissue metabolism and is dosed by depot interval, not renal function. | — Peptide depot formulation; not relevant to dialyzability and no ESKD dose change needed. The clinical focus in ESKD is cardiometabolic and bone management. |
| Lifileucel PRE Tumor-infiltrating lymphocyte (TIL) therapy | Lifileucel itself is a one-time cell infusion with no renal dose adjustment. The renal-relevant levers are the conditioning regimen: fludarabine requires dose reduction in renal impairment (it is renally cleared and accumulates), and high-dose IL-2 dosing is governed by real-time hemodynamic/organ tolerance rather than a fixed CrCl threshold. | No The TIL product is not dialyzable. Among conditioning agents, fludarabine's active metabolite is partly dialyzable but timing is not standardized; IL-2 management is hemodynamic. No established protocol exists for the regimen in dialysis-dependent patients, who are generally excluded. |
| Lomustine (CCNU) CIN Nitrosourea alkylator | Reduce or avoid in baseline renal impairment; the oral dose is given at long (~6-week) intervals partly to limit cumulative marrow and organ toxicity. Cap lifetime cumulative dose and hold for a sustained creatinine rise. | Yes Lipophilic, rapidly metabolized; not meaningfully dialyzable and dialysis is not a rescue strategy. ESKD experience is anecdotal. |
| Loncastuximab tesirine PRE Antibody-drug conjugate (CD19/PBD) | No dose adjustment for mild-moderate renal impairment; severe impairment/ESKD not well studied. As an ADC, clearance is not primarily renal. | No A large antibody-drug conjugate; not dialyzable. ESKD dosing is not established. |
| Lorlatinib PSEUDO ALK TKI | No starting-dose change for mild-to-moderate renal impairment. For severe renal impairment (eGFR <30 mL/min not on dialysis), reduce the dose (e.g., from 100 mg to 75 mg once daily) per labeling. Avoid strong CYP3A inducers/inhibitors. | — Hepatically metabolized and protein-bound; not expected to be meaningfully dialyzed, and ESKD data are limited - monitor clinically. |
| Lurbinectedin ATN Marine alkylating agent | Standard 3.2 mg/m2 IV over 1 h every 3 weeks; dose reductions to 2.6 then 2.0 mg/m2 for toxicity. No dedicated renal adjustment for mild-moderate impairment; severe renal/hepatic impairment has not been studied, so CrCl cutoffs are not established. | — Not characterized; high protein binding and a large volume of distribution make significant dialytic removal unlikely. Dialysis would be used to support AKI, not to clear drug. |
| Lutetium-177 Dotatate CIN Radioligand therapy (PRRT) | Standard course is 7.4 GBq IV every 8 weeks for 4 cycles. There is no simple CrCl-based dose table; instead activity is governed by the renal radiation-tolerance threshold (classically ~23 Gy absorbed dose; a renal BED cap of ~37-40 Gy is used in dosimetry-guided practice). Baseline CrCl <30 mL/min or rapidly declining renal function is a contraindication/caution; reduce or omit cycles for grade >=2-3 renal toxicity. | Yes Not relevant as a management strategy — the toxicity is chronic structural radiation injury, not a removable circulating drug. The amino-acid load is dialyzable but this is not clinically used. PRRT is generally not given to dialysis-dependent patients. |
| Lutetium-177 PSMA-617 (vipivotide) CIN Radioligand therapy (PSMA) | Standard 7.4 GBq IV every 6 weeks for up to 6 cycles. No simple CrCl-based table; the same ~23 Gy renal radiation-tolerance principle applies (renal dose ~0.4-0.55 Gy/GBq in dosimetry series). Hold/reduce for grade >=3 renal or hematologic toxicity; caution with significantly impaired baseline GFR. | — Not relevant as management (structural radiation effect rather than a removable drug). No established ESKD dosing; such patients are generally not candidates. |
| Mechlorethamine LYTE Alkylating agent (nitrogen mustard) | No validated renal dose-adjustment algorithm for systemic use; the drug is rapidly chemically hydrolyzed with very short plasma half-life. Topical gel requires no renal adjustment given absent systemic absorption. | — Not relevant for drug removal given near-instantaneous chemical degradation in plasma; dialysis is used only to manage TLS metabolic complications. |
| Melphalan SIADH Alkylator | For high-dose conditioning, reduce from 200 to 140 mg/m2 in significant renal impairment / dialysis dependence and in AL amyloidosis. PK studies show high-dose melphalan can be given in renal failure with acceptable toxicity at the reduced dose. | Yes Melphalan is short-lived (rapid chemical hydrolysis) so it is not reliably removed by dialysis as a rescue; however, high-dose autotransplant has been performed safely in dialysis-dependent patients using the reduced 140 mg/m2 dose with attention to mucositis. |
| Melphalan flufenamide (melflufen) ATN Peptide-conjugated alkylator | Reduced dose (30 mg) recommended for moderate renal impairment (eGFR ~30 to <45 mL/min/1.73 m2) based on the BRIDGE PK study; data in severe impairment are limited (a 20 mg dose was studied). Recalculate eGFR before dosing. | — Released melphalan is a small molecule with limited published dialyzability data for the conjugate; no established dosing in dialysis-dependent patients. Use with caution and close monitoring in advanced CKD. |
| Midostaurin PRE FLT3 / multikinase inhibitor | No specific renal dose adjustment for mild-moderate impairment; severe impairment/ESKD not well characterized (extensive hepatic CYP3A4 metabolism, highly protein-bound). Modifications driven by hematologic/GI toxicity and QT. | Yes Highly protein-bound; not expected to be dialyzable. Dialysis is used for TLS metabolic complications, not drug clearance. |
| Mirdametinib PRE MEK inhibitor | No established renal dose adjustment; mirdametinib is hepatically metabolized with low renal elimination, so reduced GFR is not expected to require modification. Dosing is BSA-based in children. No data in severe impairment or dialysis. | — Not characterized; a small, protein-bound, non-renally cleared molecule is unlikely to be appreciably dialyzed. No ESKD dosing guidance. |
| Mirvetuximab soravtansine PRE Antibody-drug conjugate (FRα/DM4) | No renal dose adjustment defined for mild-moderate impairment; data are limited in severe impairment/ESKD. DM4 is hepatically metabolized rather than renally cleared. | — Not appreciably dialyzed (large ADC; protein-bound maytansinoid payload). |
| Mitotane LYTE Adrenolytic | Mitotane dosing is guided by plasma-level monitoring and tolerability rather than by renal function; there is no standardized renal dose reduction. In EDP-M with mild renal impairment, cisplatin scheduling (e.g., continuous infusion) is modified to mitigate nephrotoxicity. | — Dialyzability not characterized/clinically relevant; mitotane is highly lipophilic and tissue-distributed, making dialysis removal unlikely to be useful. |
| Mitoxantrone PRE Anthracenedione | No well-defined renal CrCl thresholds (minimal renal elimination — predominantly hepatobiliary clearance); reduce/monitor in hepatic impairment. Cumulative dose is limited by cardiotoxicity rather than renal function. | Yes Not appreciably dialyzable (large volume of distribution and high tissue/protein binding); dialysis is used for tumor-lysis metabolic management. |
| Mobocertinib PRE EGFR exon20 TKI | Standard 160 mg PO daily. No fully established renal dose-adjustment scheme; renal management is mainly diarrhea/volume control plus dose interruption/reduction. | Yes Not characterized; a small-molecule TKI that is highly protein-bound and hepatically metabolized, so it is unlikely to be dialyzable. |
| Mogamulizumab PRE Anti-CCR4 antibody | No dose adjustment for renal impairment (a monoclonal antibody, not renally cleared); interruptions are driven by rash and infusion reactions. | No A monoclonal antibody; not dialyzable. Dialysis is used for TLS metabolic complications, not drug removal. |
| Momelotinib PRE JAK/ACVR1 inhibitor | No dose adjustment is needed for mild-to-severe renal impairment per the registrational program; momelotinib is hepatically metabolized (with an active metabolite). Data in dialysis are limited. Dose modification is driven primarily by cytopenias rather than renal function. | — Not characterized; highly protein-bound, hepatically cleared. Not expected to be meaningfully dialyzed. No ESKD-specific dosing guidance. |
| Mosunetuzumab PRE Bispecific (CD20×CD3) | No specific renal dose adjustment is defined; mild-to-moderate renal impairment is not expected to alter exposure of an IgG bispecific. No data in severe impairment/ESKD — dose on clinical grounds. | No Not dialyzable (~145 kDa IgG cleared by reticuloendothelial catabolism, not renal filtration). No supplemental dosing needed for HD/PD. |
| Moxetumomab pasudotox TMA Immunotoxin (anti-CD22 PE38) | Do not initiate if CrCl <30 mL/min. Hold for serious CLS or HUS; permanently discontinue for HUS or recurrent serious CLS. No simple CrCl-based dose scaling otherwise. | — Not characterized — dialysis supports AKI/HUS rather than clearing the immunotoxin. |
| Necitumumab LYTE Anti-EGFR antibody | No renal dose adjustment of the antibody is defined; necitumumab is not renally cleared. Management is electrolyte repletion and dose holds for severe hypomagnesemia rather than mg/kg reduction. Note the concurrent cisplatin requires its own CrCl-based dosing/hydration. | No Not dialyzable—a ~145 kDa IgG1 monoclonal antibody cleared by reticuloendothelial catabolism, not removed by hemodialysis; no supplemental dosing after HD. (Magnesium itself is small and dialyzable, but the toxicity is renal wasting, not retention.) |
| Nedaplatin ATN Platinum agent | No formally validated CrCl-banded schema in Western labeling; in practice dose is reduced and free-platinum AUC monitored when CrCl is low. Reduce dose / extend interval for baseline renal impairment and avoid stacking with cisplatin-level cumulative platinum. | Yes Free (unbound) platinum is dialyzable like other small-molecule platinums; protein-bound platinum is not. Timing of any platinum agent around hemodialysis should be individualized with pharmacy. Renal clearance is a major elimination route, so ESKD prolongs exposure. |
| Nelarabine PRE Purine analog | No specific renal dose adjustment is defined in the label, but exposure is higher and clearance lower in renal impairment, so the FDA label advises monitoring patients with CrCl < 50 mL/min closely for increased toxicity. Ara-G is renally cleared. | — Not formally established; ara-G is a small renally excreted molecule with theoretical dialytic removal, but no validated supplemental dosing exists and HD is used only to manage AKI complications. |
| Neratinib PRE HER2 / pan-EGFR TKI | No dose adjustment for mild-moderate renal impairment; severe impairment/ESKD not well studied (hepatic CYP3A4 metabolism). Dose changes are driven by diarrhea and hepatotoxicity. | Yes Highly protein-bound; not expected to be dialyzable. No established ESKD dosing. |
| Nilotinib PRE BCR-ABL TKI | No renal dose adjustment is required (negligible renal excretion); nilotinib is given without change across renal-function categories. Note the QT-prolongation black-box warning and the need to take it on an empty stomach. | No Highly protein-bound and hepatically cleared; not dialyzable and no supplemental dosing needed in ESKD. |
| Nimustine (ACNU) CIN Nitrosourea (alkylating) | Use caution in renal impairment; nimustine-specific renal dose thresholds are not well defined. Limit cumulative exposure and withhold for evolving renal dysfunction; individualize per protocol. | — Not well characterized. Although nimustine is comparatively water-soluble, it is rapidly metabolized with a short plasma half-life, so dialysis is not an established removal strategy; manage by dose limitation and monitoring. |
| Nintedanib HTN VEGFR/FGFR/PDGFR TKI | No dose adjustment for mild-to-moderate renal impairment; <1% is excreted renally and nintedanib is predominantly cleared by hydrolytic ester cleavage and biliary/fecal excretion. It has not been studied in severe renal impairment (CrCl < 30 mL/min). Dose reduction is driven by hepatotoxicity (transaminitis) more than by renal function. | Yes Highly protein-bound (~98%) with biliary/fecal elimination, so it is not meaningfully dialyzable; no supplemental dosing for HD. ESKD data are essentially absent. |
| Niraparib HTN PARP inhibitor | No formal renal dose adjustment for mild-moderate impairment; not studied in CrCl <30 mL/min or on dialysis (use with caution). Individualized starting dose (200 mg) is recommended by weight (<77 kg) and platelet count (<150,000/µL) for hematologic, not renal, safety. | Yes Small molecule but highly protein-bound (~83%) with a large volume of distribution; not expected to be meaningfully removed by hemodialysis. No validated ESKD dosing — extrapolate cautiously and prioritize cytopenia monitoring. |
| Nirogacestat LYTE Gamma-secretase inhibitor | No established renal dose adjustment; not studied in significant renal impairment. Modify dose for GI/dermatologic toxicity per label rather than for GFR. CYP3A interactions apply. | — Hepatically metabolized small molecule; dialyzability not characterized and not the management focus. In advanced CKD, monitor and replete electrolytes/phosphate. |
| Obinutuzumab XTAL Anti-CD20 antibody | No renal dose adjustment; antibody clearance is target-mediated/reticuloendothelial, not renal. CLL11 specifically included patients with CrCl 30–69 mL/min, supporting use in moderate renal impairment with appropriate TLS precautions. | No Not dialyzed — a large IgG1 antibody not removed by HD/PD; usable in ESKD at standard dosing. Dialysis treats TLS complications, not drug levels. |
| Octreotide LYTE Somatostatin analog | No adjustment for mild-to-moderate renal impairment is generally mandated, but clearance is reduced in severe impairment and in dialysis patients, where lower or less frequent dosing and closer monitoring are prudent; consult product labeling for the specific formulation. | Yes Not meaningfully removed by dialysis as a basis for supplemental dosing; the peptide is partly renally eliminated, and case experience supports cautious use in hemodialysis patients without routine post-dialysis supplementation. |
| Olaparib PRE PARP inhibitor | No starting-dose change for mild renal impairment (CrCl 51-80). For moderate impairment (CrCl 31-50), reduce the dose (e.g., to 200 mg twice daily) per labeling. Severe impairment/ESKD (CrCl <30) is not recommended due to limited data; if used, monitor closely. | — Olaparib is protein-bound and predominantly hepatically metabolized (CYP3A); dialyzability is not well characterized and it is not relied upon for clearance. Avoid in dialysis-dependent ESKD given sparse data. |
| Olutasidenib PRE IDH1 inhibitor | No dose adjustment for mild-moderate renal impairment; severe impairment/ESKD not well characterized (hepatic metabolism). Interruptions are driven by differentiation syndrome/TLS rather than GFR. | Yes Highly protein-bound; not appreciably dialyzable. Dialysis is used for TLS metabolic complications, not drug removal. |
| Osimertinib SIADH EGFR TKI | No osimertinib dose adjustment is required for mild-to-moderate renal impairment; data in severe impairment/ESKD are limited (hepatic CYP3A metabolism predominates). Management of SIADH is fluid restriction and dose hold, not renal dose modification. | Yes Not appreciably dialyzable—a small but highly lipophilic, extensively protein-bound molecule with a very large volume of distribution; minimal renal excretion of parent drug, so hemodialysis is not expected to remove clinically relevant amounts. |
| Paclitaxel PRE Taxane | Hepatically (CYP2C8/CYP3A4) metabolized and biliary excreted - no renal dose adjustment; reduce dose for significant hepatic impairment. Renal impairment does not require dose change. | No Highly protein-bound, large volume of distribution, and non-renally cleared; not dialyzable. Can be given without regard to dialysis timing. |
| Palbociclib PSEUDO CDK4/6 inhibitor | No renal dose adjustment is specified for mild-to-moderate impairment; pharmacokinetic data in severe impairment/ESKD are limited. Do not dose-reduce for an isolated creatinine rise that is actually pseudo-AKI. | Yes Highly protein-bound, large volume of distribution, and hepatically (CYP3A4) metabolized; not meaningfully removed by hemodialysis. No HD-timed dosing established. |
| Pegaspargase PRE Enzyme (asparaginase) | The enzyme is cleared by reticuloendothelial/proteolytic mechanisms, not renally excreted, so no renal dose adjustment is required. Hold or adjust for pancreatitis, serious thrombosis/hemorrhage, or severe hypersensitivity — not for creatinine. | Yes Not meaningfully dialyzable (a large PEGylated protein); hemodialysis is not used for removal. |
| Pemigatinib LYTE FGFR inhibitor | No starting-dose change for mild-moderate renal impairment; severe impairment/dialysis not well studied. Dosing is driven by the phosphate-guided algorithm (and the intermittent 14-days-on/7-days-off schedule) rather than a CrCl rule. | — Highly protein-bound oral small molecule; not expected to be appreciably dialyzed. No validated ESKD dosing; the phosphate biomarker is confounded in ESKD. |
| Pentostatin ATN Purine analog (ADA inhibitor) | Renally adjusted: CrCl >60 mL/min ~4 mg/m2 every 14 days (standard); CrCl 41-60 ~3 mg/m2; CrCl 21-40 ~2 mg/m2; CrCl <20-30/severe generally avoid (insufficient data). Even these reductions may overexpose critically ill patients (Cockcroft-Gault overestimates function) — interpret cautiously. | Yes Dialyzable — deliberate post-infusion hemodialysis has been used to limit exposure and permit cautious dosing in ESKD. |
| Pexidartinib PRE CSF1R inhibitor | No specific renal dose adjustment defined; the critical modifications are for hepatotoxicity. Use general caution in CKD; hepatic metabolism predominates. | Yes Highly protein-bound; not expected to be dialyzable. No established ESKD dosing. |
| Pirtobrutinib PRE Non-covalent BTK inhibitor | No dose adjustment for mild–moderate renal impairment; data in severe impairment/ESKD are limited (reduced dose has been studied in severe impairment per label). Hepatic and drug-interaction adjustments apply. | — Small molecule, highly protein-bound, hepatically metabolized; dialyzability not well characterized and removal unlikely to be clinically significant. Renal replacement therapy in this setting treats TLS, not drug levels. |
| Plicamycin (mithramycin) ATN Antitumor antibiotic | Contraindicated/avoided in significant renal impairment because nephrotoxicity is cumulative and dose-related; lower doses are used for hypercalcemia than for antitumor effect. No validated renal dose-adjustment schema exists given its obsolescence — the practical guidance is avoidance when renal function is impaired. | — Not characterized; dialysis is not used for dosing. Hemodialysis would be employed only to manage AKI complications, not to remove the drug. |
| Polatuzumab vedotin PRE Antibody-drug conjugate (CD79b/MMAE) | No starting-dose adjustment for CrCl >=30; data are insufficient below CrCl 30. MMAE is hepatically (CYP3A4) metabolized rather than renally cleared. | — Not appreciably dialyzed (large ADC; protein-bound MMAE). No supplemental dosing guidance for HD/PD. |
| Pomalidomide PRE Immunomodulatory drug (IMiD) | No starting-dose change is required for renal impairment, including severe CKD and dialysis (extensive hepatic metabolism). On hemodialysis, give pomalidomide after the dialysis session. Reduce dose for hepatic impairment and for hematologic toxicity. | Yes Pomalidomide is not appreciably removed by hemodialysis to a degree requiring supplemental dosing; administer the daily dose after dialysis on dialysis days. No dose reduction needed for ESKD. |
| Ponatinib HTN BCR-ABL TKI | No specific renal dose adjustment is established (minimal renal excretion); dosing is driven instead by response and by mitigation of vascular toxicity (e.g., reduce to 15 mg on achieving response). Use caution in renal impairment given the vascular risk profile. | — Highly protein-bound and hepatically metabolized; not appreciably dialyzed and no supplemental dosing required in ESKD. |
| Pralatrexate XTAL Antifolate | In the dedicated renal-impairment PK study, severe renal impairment (and ESRD on dialysis) required dose reduction (to ~15 mg/m2) owing to reduced clearance and higher exposure; mild-moderate impairment was tolerated near standard dosing with monitoring. Hold/reduce for grade 3-4 mucositis or cytopenias. | — Hemodialysis can lower pralatrexate exposure; in the renal-impairment study, dosing in ESRD patients was reduced and timed around dialysis. It is a small molecule with partial renal handling, so dialysis contributes to clearance but dose reduction remains necessary. |
| Pralsetinib HTN RET inhibitor | No dose adjustment for mild-moderate renal impairment; severe impairment is not well characterized and dialysis is not studied (use with caution). Modifications are driven by hypertension, pneumonitis, cytopenias, and hepatotoxicity. | — Highly protein-bound oral small molecule; not expected to be appreciably dialyzed. No validated ESKD dosing. |
| Procarbazine ATN Hydrazine alkylating agent | No well-validated renal dosing algorithm; use caution in renal impairment given active metabolite handling, and consider dose reduction with close monitoring. Hepatic impairment and MAO-inhibitor drug/dietary interactions are the better-defined dosing concerns. | — Dialyzability not well characterized; the parent drug is short-lived and extensively metabolized. No established ESKD dosing — manage clinically with attention to active metabolites. |
| Quizartinib PRE FLT3 inhibitor | No renal dose adjustment is specified for mild-moderate impairment; quizartinib is hepatically (CYP3A) metabolized. Note the critical CYP3A drug-interaction caveat: strong CYP3A inhibitors (common azole antifungals in neutropenia) raise exposure and require dose reduction, mainly for QT safety. Limited data in severe impairment/dialysis. | — Not characterized; highly protein-bound, hepatically cleared — not expected to be meaningfully dialyzed. No ESKD dosing guidance. |
| Radium-223 dichloride PRE Radiopharmaceutical (alpha-emitter) | Standard 55 kBq/kg IV every 4 weeks for 6 injections. No renal dose adjustment is required given negligible renal clearance and exposure; holds are driven by hematologic parameters (ANC, platelets), not CrCl. | — Not a clinical consideration — minimal renal handling and no removable nephrotoxic moiety. No ESKD-specific dosing guidance is established. |
| Raltitrexed ATN Antifolate (TS inhibitor) | Dose by creatinine clearance: full dose for CrCl >= 65 mL/min; reduce dose and lengthen the dosing interval for CrCl 25-65 mL/min (e.g., reduced dose every 4 weeks); not recommended for CrCl < 25 mL/min. Always recalculate GFR before each cycle. | Yes Polyglutamated, tissue-retained antifolate cleared largely by the kidney; not characterized as efficiently dialyzable and not recommended in dialysis-dependent patients. Use in ESKD is generally avoided. |
| Ramucirumab HTN Anti-VEGFR2 antibody | No pharmacokinetic renal dose adjustment is required for a monoclonal antibody, but dosing is modified by toxicity: interrupt/reduce for grade 3 hypertension until controlled and for proteinuria thresholds above. Renal impairment does not alter antibody clearance. | No Not dialyzable — a ~147 kDa IgG1 monoclonal antibody is not removed by hemodialysis or peritoneal dialysis; no dose change is needed for dialysis patients. |
| Regorafenib HTN VEGFR TKI | No dose adjustment for renal impairment is recommended; regorafenib is hepatically metabolized (CYP3A4 and UGT1A9) with biliary excretion, so it carries hepatotoxicity warnings rather than renal dosing rules. Renal impairment does not require dose change. | Yes Highly protein-bound (~99.5%) and hepatically/biliary cleared; not appreciably dialyzable, so no supplemental dosing for HD. Data in ESKD are limited. |
| Relatlimab AIN Immune checkpoint inhibitor (anti-LAG-3) | No renal dose adjustment is established (monoclonal antibody, not renally cleared); mild–moderate impairment does not require change. The actionable step is holding the drug and steroid treatment for immune-mediated AIN rather than dose modification. | No The IgG antibodies are not dialyzable and are cleared by proteolysis; no ESKD dose change is expected. Dialysis supports severe AKI management, not drug removal. |
| Repotrectinib PSEUDO ROS1/TRK TKI | No renal dose adjustment for mild–moderate impairment; severe impairment/ESKD not well studied. Critically, an isolated transporter-mediated creatinine rise should NOT, by itself, trigger renal dose reduction — confirm true GFR first. | — Hepatically metabolized small molecule; dialyzability not characterized and not clinically relevant to the (artifactual) creatinine rise. No established ESKD dosing. |
| Revumenib PRE Menin inhibitor | Dosed with a strong CYP3A4 inhibitor co-administration strategy in the label; no well-established renal dose adjustment. Manage TLS/differentiation syndrome rather than adjust for GFR; hold for severe differentiation syndrome. | — Small molecule, but renal dialyzability not formally characterized; clinically, renal replacement therapy is used for TLS-driven AKI/refractory hyperkalemia, not for drug removal. |
| Ribociclib PSEUDO CDK4/6 inhibitor | No adjustment for mild-moderate renal impairment; the label provides a reduced starting dose (e.g. 200 mg) for severe impairment. Avoid strong CYP3A4 inhibitors or reduce dose accordingly. | Yes Extensively hepatically metabolized (CYP3A4), highly protein-bound; not expected to be removed by hemodialysis. No HD-timed dosing established. |
| Ripretinib HTN KIT switch-control inhibitor | No dose adjustment for mild-moderate renal impairment in labeling; severe impairment/ESKD not characterized (hepatic CYP3A4 metabolism). Modifications driven by hypertension, PPE and cardiac effects. | Yes Highly protein-bound; not expected to be dialyzable. No established ESKD dosing. |
| Rituximab XTAL Anti-CD20 antibody | No renal dose adjustment; as a monoclonal antibody it is cleared by reticuloendothelial/target-mediated mechanisms, not the kidney, and is dosed by BSA/flat dose regardless of CrCl. Renal function changes are driven by the tumor-lysis risk it provokes, not by drug accumulation. | No Not dialyzed — a ~145 kDa IgG1 antibody is not removed by hemodialysis or peritoneal dialysis. No supplemental dosing around dialysis; usable in ESKD at standard doses. Dialysis is used to treat TLS metabolic complications. |
| Rucaparib PRE PARP inhibitor | No starting-dose adjustment for mild-moderate renal impairment (CrCl >=30 mL/min); not studied in CrCl <30 mL/min or dialysis — use with caution. Modest exposure increases occur with moderate impairment but rarely require dose change. | — Highly protein-bound small molecule; not expected to be appreciably dialyzed. No established ESKD dosing. |
| Ruxolitinib PRE JAK1/2 inhibitor | Renal dosing is required: the starting dose is reduced in moderate-to-severe renal impairment and in ESKD. In myelofibrosis/PV with platelets 100-150 x10^9/L and severe impairment (CrCl 15-29), and in dialysis-dependent ESKD, the label specifies reduced starting doses; in ESKD on hemodialysis, give a single reduced dose after dialysis on dialysis days. Always titrate to platelets and response. | Yes Ruxolitinib and its active metabolites are not efficiently removed by hemodialysis; dose AFTER dialysis on HD days. Highly protein-bound, hepatically (CYP3A4) metabolized small molecule. |
| Sacituzumab govitecan PRE Antibody-drug conjugate (Trop-2/SN-38) | No established renal dose adjustment; pivotal trials did not define renal cutoffs and the active SN-38 is hepatically glucuronidated (UGT1A1), not renally cleared. Use clinical judgment in advanced CKD/ESKD given limited data. | — The intact ADC and protein-bound SN-38 are not appreciably dialyzed; HD in reported cases was for AKI support, not drug removal. |
| Samarium-153 lexidronam ATN Bone-seeking radiopharmaceutical (153Sm-EDTMP) | Renal impairment reduces clearance and increases marrow radiation exposure; administer with caution and assess renal function before dosing. Follow product labeling/nuclear-medicine guidance for impaired renal function. | — Not established as a removal modality; clinical role of dialysis is supportive only. |
| Selinexor SIADH XPO1 (nuclear export) inhibitor | Limited renal data; no dedicated adjustment for mild-moderate renal impairment is established, and severe CKD/dialysis are not well studied — individualize with onconephrology input. Dose is otherwise modified for hyponatremia and cytopenias. | Yes Not established; highly protein-bound and not expected to be meaningfully dialyzable. |
| Selpercatinib HTN RET inhibitor | No dose adjustment for mild-moderate renal impairment; severe impairment is not well characterized and dialysis is not studied (use with caution). Weight-based dosing; modifications are driven by hypertension, QTc, hepatotoxicity, and hemorrhage. | — Highly protein-bound oral small molecule; not expected to be appreciably dialyzed. No validated ESKD dosing. |
| Selumetinib PRE MEK inhibitor | Weight/BSA-based pediatric dosing; no specific renal adjustment established (renal-impairment data are limited in this young population). Hepatic impairment, not renal, carries label dose guidance. | — Highly protein-bound oral small molecule; dialyzability not characterized and not clinically relevant in this indication. No ESKD dosing data. |
| Sirolimus GLOM mTOR inhibitor | No mandatory dose reduction for renal impairment per se (sirolimus is hepatically metabolized via CYP3A4), but troughs should be kept toward the lower end and proteinuria monitored when GFR is reduced. Avoid initiating or escalating in the setting of significant proteinuria or progressive glomerular disease. | Yes Not meaningfully dialyzable—sirolimus is large, highly lipophilic, extensively (~92%) protein/erythrocyte bound with a very large volume of distribution; hemodialysis does not remove clinically relevant amounts and no supplemental dosing is needed after HD. |
| Sonidegib ATN Hedgehog (SMO) inhibitor | No specific renal dose adjustment in labeling for mild-moderate impairment; not studied in severe impairment/ESKD. Dosing is fixed (200 mg daily); modifications are driven by musculoskeletal toxicity/CK. | Yes Highly protein-bound; not meaningfully dialyzable. Hemodialysis is used for the metabolic complications of pigment-induced ATN, not to remove the drug. |
| Sotorasib PRE KRAS G12C inhibitor | No renal dose adjustment is recommended; sotorasib pharmacokinetics were not meaningfully affected by mild-moderate renal impairment, and severe impairment/ESKD are not well studied. Dose modifications (from 960 mg daily) are driven by hepatotoxicity and GI toxicity, not CrCl. | — Not characterized; as a highly protein-bound, hepatically cleared small molecule it is unlikely to be substantially dialyzed. No ESKD dosing guidance is established. |
| Streptozocin FANC Nitrosourea alkylator | Reduce dose and lengthen interval for impaired renal function; hold for new or worsening proteinuria or rising creatinine. Modern reviews emphasize scheduling (lower per-dose, fractionated) to cap cumulative tubular exposure in pNET. | — Small, renally cleared molecule; specific HD removal data are limited and it is rarely used in ESKD. Avoid in significant renal impairment rather than relying on dialytic clearance. |
| Strontium-89 chloride LYTE Bone-seeking radiopharmaceutical | No standardized renal dose-reduction scheme; instead, renal impairment is a caution/relative contraindication because reduced clearance increases retained activity and marrow exposure. Dosing is activity-based (e.g., ~150 MBq) per protocol with attention to baseline counts and renal function. | Yes Not a standard management consideration; once incorporated into bone mineral, strontium-89 is not meaningfully removed by dialysis. Early circulating/urinary fraction is renally handled, but dialysis is not used as antidotal clearance. |
| Sunvozertinib SIADH EGFR exon20 TKI | No dedicated renal dose adjustment established; sunvozertinib is hepatically metabolized (CYP3A) with low renal clearance, so mild-moderate impairment is not expected to require change. Limited data in severe impairment/dialysis. | — Not characterized; a highly protein-bound, non-renally cleared small molecule is unlikely to be appreciably dialyzed. No ESKD dosing guidance. |
| Tafasitamab PRE Anti-CD19 antibody | No dose adjustment for renal impairment for the antibody (not renally cleared); the lenalidomide partner does require CrCl-based dose adjustment. Manage tafasitamab interruptions for infusion reactions/cytopenias. | No A monoclonal antibody; not dialyzable. ESKD dosing of the antibody is not specifically established; lenalidomide needs renal dose adjustment. |
| Tagraxofusp PRE IL-3 immunotoxin | No established renal dose adjustment (clearance is proteolytic, not renal). Dosing decisions hinge on albumin, weight, and CLS status rather than eGFR. | No Large fusion protein cleared by proteolysis; not dialyzable. Hemodialysis/CRRT is used to support AKI/volume overload, not to remove the drug. |
| Talazoparib PRE PARP inhibitor | Breast-cancer monotherapy: CrCl 60-89 no change; CrCl 30-59 reduce to 0.75 mg once daily; CrCl 15-29 reduce to 0.5 mg once daily. With enzalutamide in mCRPC, label-specific lower doses apply. Not studied on dialysis or in CrCl <15 mL/min. | — Renally cleared but highly protein-bound; dialyzability not formally established and no validated ESKD dose — avoid or use only with intensive hematologic monitoring. |
| Talquetamab PRE Bispecific (GPRC5D×CD3) | No specific renal dose adjustment is established; talquetamab pharmacokinetics are not meaningfully renally dependent. Step-up dosing and holds for severe CRS, plus supportive management of oral toxicity, are the operative levers rather than renal dose modification. | No Not dialyzable—an IgG-based bispecific antibody cleared by catabolism; not removed by hemodialysis and no supplemental dosing needed. Renal replacement therapy treats AKI, not drug clearance. |
| Tamoxifen SIADH SERM | No renal dose adjustment required; tamoxifen is hepatically metabolized (CYP2D6/3A4) and not renally cleared. | No Highly protein-bound, large volume of distribution, hepatically cleared — not dialyzable. No special ESKD dosing needed. |
| Tarlatamab PRE Bispecific (DLL3×CD3) | No established renal dose adjustment (T-cell engager, not renally cleared); dosing is by step-up schedule. The renal-relevant action is hemodynamic support during CRS, not dose modification for GFR. | No Bispecific antibody construct — not dialyzable and not renally eliminated; no ESKD dose change expected. Renal replacement therapy is for CRS-driven AKI, not drug clearance. |
| Tazemetostat PRE EZH2 inhibitor | No specific renal dose adjustment defined for mild-moderate impairment; severe impairment/ESKD not characterized (hepatic CYP3A metabolism). Modifications relate to hematologic toxicity and the secondary-malignancy risk. | Yes Highly protein-bound; not expected to be dialyzable. Dialysis is used for TLS metabolic complications, not drug removal. |
| Tebentafusp PRE Bispecific T-cell engager (gp100×CD3 ImmTAC) | No dedicated renal dose adjustment is established; the fixed weekly step-up schedule is driven by CRS mitigation, not renal function. Manage AKI by hemodynamic support rather than dose change. | No The engineered TCR-anti-CD3 fusion protein is not dialyzable in a clinically meaningful sense; no ESKD dose change is defined. Dialysis would support AKI management, not drug removal. |
| Teclistamab PRE Bispecific (BCMA×CD3) | No specific renal dose adjustment is established; teclistamab pharmacokinetics are not meaningfully renally dependent, and patients with renal impairment (including some on dialysis) have been treated. The operative levers are step-up dosing and holds for severe CRS rather than renal dose modification. | No Not dialyzable—an IgG-based bispecific antibody cleared by catabolism; not removed by hemodialysis and no supplemental dosing needed. Renal replacement therapy, if used, treats AKI, not drug clearance. |
| Tegafur-uracil (UFT) TMA Antimetabolite (oral 5-FU prodrug) | No universally validated renal dosing nomogram. Because 5-FU and metabolites have a renal elimination component, use caution and consider dose reduction in significant renal impairment; follow regional product labeling. | — Not well characterized for the tegafur/uracil combination; dialysis is used to support AKI rather than to remove drug. |
| Temozolomide SIADH Alkylator | No renal dose adjustment is established; temozolomide pharmacokinetics are dominated by non-renal chemical degradation. Standard dosing is used across normal-to-mild renal impairment, with caution and limited data in severe impairment/dialysis. | — Short half-life with predominantly non-renal (spontaneous hydrolysis) elimination; not a drug managed by dialysis. Limited ESKD data, but renal clearance contributes little to total elimination. |
| Teniposide LYTE Podophyllotoxin (topo II) | No standardized renal dose-reduction schema is well established given low renal clearance; use caution and consider individualized reduction in severe renal or hepatic impairment and with marked hypoalbuminemia. Follow local protocol. | Yes Not meaningfully dialyzable: extensive (>99%) plasma protein binding and a relatively small free fraction make removal by hemodialysis negligible. Do not rely on dialysis for clearance. |
| Tepotinib PSEUDO MET inhibitor | No starting-dose adjustment for mild-moderate renal impairment; severe impairment and dialysis are not well studied (use with caution). Modifications are driven by edema, ILD/pneumonitis, and hepatotoxicity. | — Highly protein-bound oral small molecule; not expected to be appreciably dialyzed. No validated ESKD dosing. |
| Thalidomide PRE Immunomodulatory drug (IMiD) | No specific renal dose adjustment is mandated (thalidomide is poorly renally cleared, eliminated largely by non-enzymatic hydrolysis); use cautiously and titrate to tolerance in advanced CKD. Dose on dialysis days after the session. | No Not significantly dialyzed in routine practice; no supplemental dosing required. Give after hemodialysis on dialysis days. |
| Thiotepa CYST Alkylator | Renal impairment increases thiotepa and TEPA exposure, so caution and consideration of dose reduction are warranted in moderate-to-severe impairment; no rigidly validated CrCl band exists. Exposure is best managed by clinical PK awareness rather than a fixed formula. | — Small, lipophilic, rapidly cleared; specific HD-removal data are limited and dialysis is not used for drug clearance. In ESKD, exposure considerations argue for cautious dosing rather than reliance on dialysis. |
| Tisotumab vedotin PRE Antibody-drug conjugate (tissue factor/MMAE) | No renal dose adjustment is established; not studied in severe impairment/ESKD. Modify/hold for ocular, bleeding and other toxicities per label. | No The IgG–MMAE conjugate is not dialyzable; released MMAE is highly protein-bound and not meaningfully removed by dialysis. No ESKD dosing guidance exists. |
| Tivozanib HTN VEGFR TKI | No dose adjustment for mild-to-moderate renal impairment; tivozanib has not been studied in severe renal impairment, and it is primarily hepatically metabolized, so renal dosing rules are minimal. Monitor closely if used in advanced CKD. | Yes Highly protein-bound with a long half-life and hepatic clearance; not appreciably dialyzable and not adjusted for HD. Data in dialysis patients are sparse. |
| Topotecan PRE Topoisomerase I inhibitor | IV topotecan: no change for CrCl >=40 mL/min; reduce dose for CrCl 20-39 mL/min. Oral topotecan PK data support reduced doses in moderate-severe impairment. Insufficient data for CrCl <20 mL/min. | — Low molecular weight and renally cleared, so some removal by hemodialysis is plausible, but formal HD-timed dosing is not established; if used in dialysis patients, reduce dose and monitor counts closely. |
| Tovorafenib PRE Type II RAF inhibitor | No established renal dose adjustment; tovorafenib is hepatically metabolized with low renal elimination, so meaningful exposure change with reduced GFR is not expected. Pediatric dosing is body-surface-area based and unchanged for renal function in label-described populations. | — Not characterized; as a highly protein-bound small molecule with non-renal clearance it is unlikely to be appreciably dialyzed. No dialysis dosing data in this pediatric population. |
| Trabectedin ATN Marine alkylating agent | Standard 1.5 mg/m2 IV over 24 h every 3 weeks. Dose modification is gated by bilirubin/hepatic function, not CrCl; avoid in severe hepatic impairment. No established CrCl-based reduction; it has not been studied in CrCl <30 mL/min, so use caution. | No Not dialyzable — ~94-98% protein-bound with a large volume of distribution and predominantly biliary elimination (<10% urinary). Dialysis is used to support AKI, not to remove the drug. |
| Trastuzumab deruxtecan ATN Antibody-drug conjugate (HER2/DXd) | No starting-dose adjustment for mild-moderate renal impairment; data are insufficient in severe impairment (CrCl <30) and ESKD, where higher GI/marrow toxicity has been observed and caution is advised. The cytotoxic DXd is hepatically metabolized (CYP3A4). | — Intact ADC and protein-bound DXd are not appreciably dialyzed. No supplemental dosing guidance established for HD/PD. |
| Trastuzumab emtansine (T-DM1) TMA Antibody-drug conjugate (HER2/DM1) | No starting-dose adjustment for mild-moderate renal impairment; data are lacking in severe impairment/ESKD. DM1 is hepatically metabolized; thrombocytopenia and hepatotoxicity (not renal clearance) drive most dose modifications. | — Not appreciably dialyzed (large ADC; non-cleavable linker, hepatically handled payload). |
| Tretinoin (ATRA) PRE Retinoid (differentiating agent) | No established renal dose adjustment; standard induction is 45 mg/m²/day. Dose interruptions are driven by differentiation syndrome, pseudotumor cerebri and hepatotoxicity rather than CrCl. | — Not characterized; ATRA is highly protein-bound and hepatically metabolized (and autoinduces its own metabolism), so it is not expected to be appreciably dialyzed. Dialysis, if needed, treats the AKI/fluid overload, not drug levels. |
| Trifluridine/tipiracil LYTE Oral fluoropyrimidine + TP inhibitor | No adjustment for mild renal impairment (CrCl 60-89 mL/min); for moderate impairment (CrCl 30-59) reduce the starting dose per current label; for severe impairment (CrCl 15-29) use a further-reduced dose (20 mg/m2 twice daily in the PK study). Not studied in ESKD/dialysis — avoid or use with extreme caution. | — Tipiracil is renally cleared and its dialyzability is not well characterized; no established dosing in dialysis-dependent patients. Use is generally avoided in ESKD. |
| Tucatinib PSEUDO HER2 TKI | No renal dose adjustment for mild-moderate impairment. Importantly, the creatinine rise is NOT a reason to reduce tucatinib; but it can falsely lower estimated CrCl and inappropriately trigger capecitabine dose reduction — use cystatin C-based GFR or measured GFR for companion-drug dosing decisions. Limited data in severe impairment. | — Not characterized; highly protein-bound, hepatically (CYP2C8/3A) cleared small molecule, unlikely to be appreciably dialyzed. No ESKD dosing data. |
| Vandetanib HTN VEGFR/EGFR/RET TKI | Reduce the starting dose for moderate-to-severe renal impairment per label (e.g., 200 mg when CrCl < 50 mL/min) because vandetanib is partly renally excreted and exposure rises with impairment; titrate with ECG and electrolyte monitoring. | Yes Long half-life (~19 days), large volume of distribution and high protein binding make it essentially non-dialyzable; HD does not provide meaningful removal and is not used for dosing. |
| Venetoclax XTAL BCL-2 inhibitor | No dose adjustment for mild-to-moderate renal impairment; in severe impairment (CrCl <30) and dialysis, data are limited and patients warrant intensified TLS prophylaxis/monitoring because reduced clearance of urate and phosphate magnifies TLS risk rather than because venetoclax itself accumulates renally (it is hepatically cleared). | — Not meaningfully dialyzed — highly protein-bound (>99%), hepatically (CYP3A) metabolized small molecule with negligible renal excretion. Dialysis is used to treat TLS metabolic complications, not to remove the drug. |
| Vinblastine SIADH Vinca alkaloid | Hepatically metabolized (CYP3A) and biliary excreted - no renal dose adjustment; reduce for hepatic impairment/hyperbilirubinemia. Never give intrathecally. | No Large volume of distribution and extensive tissue binding; not dialyzable. Manage hyponatremia with fluid/sodium strategies. |
| Vincristine SIADH Vinca alkaloid | Hepatically (CYP3A) metabolized and biliary excreted - no renal dose adjustment. Reduce dose for hepatic dysfunction/hyperbilirubinemia. Note the absolute dose cap to limit neurotoxicity; never administer intrathecally (fatal). | No Highly tissue-bound with a very large volume of distribution; not dialyzable. Hyponatremia is managed with fluid/sodium strategies, not dialysis. |
| Vinflunine LYTE Vinca alkaloid | Per phase I PK data: 320 mg/m2 for CrCl >=60 mL/min; 280 mg/m2 for CrCl 40 to <60 mL/min; 250 mg/m2 for CrCl 20 to <40 mL/min. These bands yield exposure comparable to patients with normal renal function. | No Not established as dialyzable in routine practice; vinflunine is largely hepatically metabolized (CYP3A4) with a large volume of distribution, making meaningful dialytic removal unlikely. Manage by dose banding, not dialysis timing. |
| Vinorelbine SIADH Vinca alkaloid | Hepatically metabolized (CYP3A) and biliary excreted - no renal dose adjustment; reduce for hepatic impairment/hyperbilirubinemia. Never give intrathecally. | No Extensive tissue binding and large volume of distribution; not dialyzable. Hyponatremia is managed by fluid/sodium strategies. |
| Vismodegib SIADH Hedgehog (SMO) inhibitor | No dose adjustment recommended for mild-moderate renal impairment; not formally studied in severe impairment/ESKD. Hepatic metabolism predominates and dosing is fixed (150 mg daily). | Yes Very highly protein-bound (>99%); not expected to be dialyzable and no ESKD dosing established. |
| Zanidatamab PRE HER2 bispecific antibody | No dedicated renal dose adjustment is specified; as a ~150 kDa monoclonal-type bispecific, clearance is not renal and exposure is not expected to change meaningfully with reduced GFR. No data in dialysis. Manage by holding/resuming for toxicity rather than CrCl-based reduction. | No Not dialyzable — large bispecific antibody cleared by reticuloendothelial proteolysis, not removed by hemodialysis or peritoneal dialysis. No ESKD-specific dosing guidance exists; standard dosing is reasonable with attention to volume status during infusion. |
| Zanubrutinib PRE BTK inhibitor | No dose adjustment for mild-to-moderate renal impairment; in severe renal impairment and on dialysis, exposure changes are modest and no dose adjustment is generally required, though data are limited. Hepatic impairment, not renal, drives reduction; minimal renal excretion of unchanged drug. | Yes Not meaningfully dialyzable — highly protein-bound, hepatically (CYP3A) cleared small molecule. No supplemental post-HD dose needed. |
| Ziftomenib PRE Menin inhibitor (investigational) | No dedicated renal dose adjustment is established; ziftomenib is hepatically metabolized. Dose interruption is driven by differentiation syndrome, QTc and cytopenias rather than CrCl. Data in significant renal impairment/dialysis are absent. | — Not characterized; a protein-bound, hepatically cleared small molecule unlikely to be appreciably dialyzed. No ESKD dosing guidance. |
| Ziv-aflibercept HTN VEGF trap | No pharmacokinetic renal dose adjustment for a fusion-protein decoy; dose modification is driven by proteinuria thresholds and hypertension grade. Renal impairment does not alter clearance of the Fc-fusion molecule. | No Not dialyzable — a ~115 kDa Fc-fusion protein is not removed by hemodialysis or peritoneal dialysis; no dose change for dialysis patients. |
| Zolbetuximab PRE Anti-Claudin-18.2 monoclonal antibody | No dedicated renal dose adjustment is established; mild–moderate impairment does not require change and severe impairment/ESKD are not well studied. Management is antiemetic control and volume repletion rather than fixed renal dosing. | No The IgG1 antibody is not dialyzable and is cleared by proteolysis; no ESKD dose change is defined. Dialysis would support AKI management, not drug removal. |
| Zongertinib PSEUDO HER2 TKI | Not formally established; as a hepatically metabolized small molecule, meaningful renal-clearance dependence is not expected. A creatinine rise attributable to transporter inhibition should not by itself trigger dose reduction. Data in significant renal impairment/dialysis are absent. | — Not characterized; protein-bound, non-renally cleared — unlikely to be appreciably dialyzed. No ESKD dosing guidance. |
A teaching reference, not a dosing calculator — always confirm against the current prescribing information and your institutional protocol before adjusting therapy. Thresholds are summarized from each agent’s profile and its cited sources.