How should kidney function be monitored during Pacritinib therapy?

Serum electrolytes — especially potassium and magnesium — at baseline and regularly, with prompt repletion (heightened importance because pacritinib prolongs the QT interval); Serum creatinine/BUN and volume/orthostatic status during and after diarrhea episodes; Stool frequency and severity, plus body weight, as an early marker of impending volume loss; ECG/QTc, particularly when electrolytes are deranged or with concomitant QT-prolonging drugs; Complete blood count (thrombocytopenia and anemia are the on-target hematologic effects); Serum creatinine and eGFR at baseline and periodically.

How can kidney injury from Pacritinib be prevented?

Start proactive antidiarrheal therapy (e.g., loperamide) at the first onset of diarrhea Encourage oral hydration and actively maintain volume status Replete potassium and magnesium promptly when low Review and minimize concomitant diuretics, RAAS blockers, and other nephrotoxins Interrupt or reduce the pacritinib dose per label for severe or refractory diarrhea before prerenal injury develops Avoid strong CYP3A4 inhibitors/inducers that alter pacritinib exposure

Who is at higher risk of kidney injury from Pacritinib?

Severe or persistent diarrhea (grade 3-4) and concurrent nausea/vomiting limiting oral rehydration; Baseline volume depletion or poor oral intake; Concomitant diuretics, ACE inhibitors/ARBs, or other nephrotoxins; Older age and pre-existing chronic kidney disease; Co-administration of other QT-prolonging drugs (electrolyte-arrhythmia interplay); Advanced myelofibrosis with poor performance status.

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Printable monograph

JAK2/ACVR1 inhibitor

Pacritinib

Q: What kind of kidney injury does Pacritinib cause?

Prerenal / Hemodynamic AKI — Renal hypoperfusion from capillary leak and cytokine storm — IL-2 and CAR-T cytokine release syndrome. Other reported patterns: Electrolyte Disturbance, Acute Tubular Necrosis.

Q: Is kidney injury from Pacritinib reversible?

Reversible. Typical onset: Diarrhea is an early effect, typically emerging within the first days-to-weeks of therapy and most pronounced over roughly the first 8 weeks; it tends to be self-limited and to improve with continued treatment, antidiarrheals, and dose management. Any prerenal azotemia and electrolyte disturbance tracks the diarrhea temporally and is therefore early and episodic rather than cumulative or delayed..

Q: Is Pacritinib removed by dialysis?

Not established. Pacritinib is a highly protein-bound, hepatically (CYP3A4) metabolized small molecule, so meaningful removal by hemodialysis is unlikely and no formal dialysis-clearance data are available — and the label directs avoiding use at eGFR <30 mL/min, so ESKD dosing does not arise. If AKI develops on therapy, manage it by treating the diarrhea and the volume/electrolyte disturbance rather than by timing doses around dialysis sessions.

Vonjo · PAC

JAK2/ACVR1 inhibitor · approved 2022 · 7 citations

Up to date· through 2025

Deeply sourced7/9 · 6 signals

Met: 7 citations
Not met: 12+ references
Met: Accrued over 10+ years (span: 10y)
Met: Beyond single case reports
Met: High-impact journal
Met: Landmark reference
Met: Current through 2025
Not met: Real-world FAERS signal

Describes how this page is sourced, not how dangerous the drug is. Thinly sourced means fewer of the sourcing signals are met — not that the agent is kidney-safe. A rule-based summary, not a formal certainty appraisal.

A JAK2/IRAK1/ACVR1 inhibitor for cytopenic myelofibrosis whose kidney risk is indirect — severe diarrhea drives volume and electrolyte depletion into prerenal azotemia, not intrinsic nephrotoxicity.

ModerateJAK2/IRAK1 inhibitor

Intermediate- or high-risk primary myelofibrosis in adults with platelet count below 50 x 10^9/L (US accelerated approval, Feb 2022)Intermediate- or high-risk secondary (post-polycythemia vera or post-essential thrombocythemia) myelofibrosis with platelets below 50 x 10^9/LSecond-line myelofibrosis after ruxolitinib, particularly in the setting of treatment-limiting thrombocytopenia

§01

Signature kidney injury

Signature lesion

Prerenal / Hemodynamic AKI

Pacritinib has no established intrinsic nephrotoxicity; its renal risk is a downstream consequence of its dominant gastrointestinal toxicity. Diarrhea is the signature adverse effect — in the phase 2 study grade 1/2 diarrhea occurred in ~69% of patients and nausea in ~49% (Komrokji 2015), and in the PERSIST-1 phase 3 trial grade 3-4 diarrhea occurred in ~5%. In real-world FAERS pharmacovigilance, gastrointestinal disorders were the top disproportionality system-organ-class and diarrhea the most-reported preferred term (Zhang 2025). High-volume diarrhea (often with nausea/vomiting) can precipitate volume depletion, hypokalemia/hypomagnesemia, and prerenal azotemia, but a specific incidence of pacritinib-attributable acute kidney injury has not been separately quantified — so no headline AKI rate is quoted here.Source: 25762180

Onset & rechallenge

Time to injurySubacute (~1–6 weeks)

Diarrhea (and the prerenal azotemia/electrolyte loss that tracks it) emerges within the first days-to-weeks and is most pronounced over roughly the first 8 weeks — early and episodic, not cumulative.

Distilled from: “Diarrhea is an early effect, typically emerging within the first days-to-weeks of therapy and most pronounced over roughly the first 8 weeks; it tends to be self-limited and to improve with continued treatment, antidiarrheals, and dose management. Any prerenal azotemia and electrolyte disturbance tracks the diarrhea temporally and is therefore early and episodic rather than cumulative or delayed.” · PMID 25762180 (opens PubMed in a new tab)

§02

Renal toxicities, ranked

This agent's kidney lesions ordered by prominence — the #1 signature lesion first, then secondary and rare patterns. Cited incidence is shown where a citable figure exists; otherwise the tier stands qualitatively.

Prerenal / Hemodynamic AKI#1 · Signaturequalitative — no citable incidence
Renal hypoperfusion from capillary leak and cytokine storm — IL-2 and CAR-T cytokine release syndrome.
Electrolyte DisturbanceSecondaryqualitative — no citable incidence
Renal electrolyte derangement — magnesium/potassium/calcium wasting (cisplatin, anti-EGFR antibodies) or retention (FGFR-inhibitor hyperphosphatemia, tumor-lysis hyperkalemia/hyperphosphatemia).
Acute Tubular NecrosisSecondaryqualitative — no citable incidence
Direct death of tubular epithelial cells — the dose-limiting lesion of the platinums and zoledronate.

Toxicity fingerprint

Tap a signature to trace where it strikes the nephron.

Incidence not quantified

SeverityModerate

ReversibilityReversible

Evidence7 citations

Nephron map

Vasculature / Endothelium

Proximal Tubule

Distal Tubule / Collecting Duct

Prerenal / Hemodynamic AKI

Renal hypoperfusion from capillary leak and cytokine storm — IL-2 and CAR-T cytokine release syndrome.

§03

Kidney injury

Mechanism of kidney injury

Indirect and hemodynamic/volume-mediated rather than a direct nephron lesion. Pacritinib's JAK2/IRAK1/ACVR1 inhibition drives frequent, sometimes high-volume diarrhea (with nausea and vomiting), producing gastrointestinal fluid and electrolyte losses. The resulting extracellular volume depletion lowers renal perfusion and glomerular filtration, yielding prerenal (functional) azotemia; compensatory renin-angiotensin-aldosterone activation then enhances distal-nephron potassium secretion, compounding the direct GI losses of potassium and magnesium to produce hypokalemia and hypomagnesemia. If hypoperfusion is severe or prolonged, prerenal azotemia can progress to ischemic acute tubular necrosis. No direct tubular, glomerular, interstitial, or crystal-forming renal toxicity has been characterized for pacritinib.

Clinical presentation

Rising creatinine and BUN with a bland urine sediment and a low fractional excretion of sodium in a patient with frequent watery stools, weight loss, orthostatic symptoms, and clinical signs of volume depletion. Laboratory hypokalemia and hypomagnesemia are common and clinically important because pacritinib prolongs the QT interval, so electrolyte depletion compounds arrhythmia risk. Severe cases show oliguria and overt hypovolemia; the BUN:creatinine ratio is often elevated, consistent with a prerenal state.

Management

Largely supportive and directed at the gastrointestinal driver: control diarrhea with antidiarrheals, restore intravascular volume with oral or IV fluids, and aggressively replete potassium and magnesium (important given concurrent QT prolongation). Hold pacritinib for severe (grade 3-4) or refractory diarrhea and resume at a reduced dose once it resolves, per the prescribing information. Correcting the prerenal physiology typically lets the creatinine recover, because the injury is functional rather than structural — there is no drug-specific renal therapy. If creatinine does not improve with volume repletion, evaluate for additive or alternative causes of AKI (sepsis in an immunocompromised/thrombocytopenic host, other nephrotoxins, ischemic ATN).Lesion-level management framework

Risk factors

Severe or persistent diarrhea (grade 3-4) and concurrent nausea/vomiting limiting oral rehydration
Baseline volume depletion or poor oral intake
Concomitant diuretics, ACE inhibitors/ARBs, or other nephrotoxins
Older age and pre-existing chronic kidney disease
Co-administration of other QT-prolonging drugs (electrolyte-arrhythmia interplay)
Advanced myelofibrosis with poor performance status

Prevention

Start proactive antidiarrheal therapy (e.g., loperamide) at the first onset of diarrhea
Encourage oral hydration and actively maintain volume status
Replete potassium and magnesium promptly when low
Review and minimize concomitant diuretics, RAAS blockers, and other nephrotoxins
Interrupt or reduce the pacritinib dose per label for severe or refractory diarrhea before prerenal injury develops
Avoid strong CYP3A4 inhibitors/inducers that alter pacritinib exposure

Anticancer mechanism· how it treats cancer

Oral small-molecule kinase inhibitor with activity against JAK2 (including the JAK2 V617F mutant), FLT3, IRAK1, and ACVR1 (ALK2), while notably sparing JAK1. By dampening constitutive JAK2-STAT signaling it reduces splenomegaly and constitutional symptoms of myelofibrosis; because it spares JAK1, it can be dosed in patients with severe thrombocytopenia in whom ruxolitinib and fedratinib worsen cytopenias. Potent ACVR1 inhibition suppresses hepcidin production, contributing an anemia/transfusion-independence benefit, and IRAK1 inhibition attenuates NF-kB-driven inflammatory signaling.

Note · Renal risk is inferred from pacritinib's well-documented gastrointestinal (diarrhea) toxicity and its predictable volume/electrolyte sequelae; a pacritinib-specific AKI incidence has not been directly quantified in the literature, so the incidence above is stated qualitatively rather than as a single rate. Confirm dosing, renal, and QT guidance against the current Vonjo prescribing information.

§04

Clinical depth

Renal dose adjustment

There is no filtration-based renal dose rule for the kidney injury itself — the actionable lever is holding or reducing pacritinib for severe diarrhea (grade 3-4) or clinically significant volume/electrolyte depletion, then resuming at a reduced dose per the label. Pharmacokinetically, pacritinib is cleared predominantly by hepatic CYP3A4 metabolism with limited renal excretion, so no dose reduction is required for mild-to-moderate renal impairment; the label directs avoiding pacritinib in severe renal impairment (eGFR <30 mL/min), where PK and safety data are lacking. Avoid strong CYP3A4 inhibitors and inducers. Confirm all thresholds against the current prescribing information.

Dialyzability & ESKD dosing

Not established. Pacritinib is a highly protein-bound, hepatically (CYP3A4) metabolized small molecule, so meaningful removal by hemodialysis is unlikely and no formal dialysis-clearance data are available — and the label directs avoiding use at eGFR <30 mL/min, so ESKD dosing does not arise. If AKI develops on therapy, manage it by treating the diarrhea and the volume/electrolyte disturbance rather than by timing doses around dialysis sessions.

Differential diagnosis

The picture is prerenal/functional AKI from GI volume loss: bland sediment, low FENa (<1%), an elevated BUN:creatinine ratio, and creatinine that corrects with volume repletion distinguish it from intrinsic tubular injury. Suspect ischemic ATN if hypoperfusion was severe or prolonged (muddy-brown granular casts, FENa >2%, slower recovery despite volume). Unlike some myeloproliferative-neoplasm therapies, tumor-lysis-related urate/phosphate nephropathy is not a typical pacritinib effect. Also exclude concurrent nephrotoxins, sepsis in a thrombocytopenic/immunocompromised host, and contrast exposure, and separate diarrhea-driven hypokalemia from diuretic effect or other potassium-wasting causes.

Monitoring

Serum electrolytes — especially potassium and magnesium — at baseline and regularly, with prompt repletion (heightened importance because pacritinib prolongs the QT interval)
Serum creatinine/BUN and volume/orthostatic status during and after diarrhea episodes
Stool frequency and severity, plus body weight, as an early marker of impending volume loss
ECG/QTc, particularly when electrolytes are deranged or with concomitant QT-prolonging drugs
Complete blood count (thrombocytopenia and anemia are the on-target hematologic effects)
Serum creatinine and eGFR at baseline and periodically

Key trials & series

PERSIST-2 (Mascarenhas 2018, JAMA Oncol) — registrational phase 3 in myelofibrosis with platelets <=100 x 10^9/L; basis for the 200 mg twice-daily accelerated approval, with diarrhea among the most common adverse events.
PERSIST-1 (Mesa 2017, Lancet Haematol) — phase 3 versus best available therapy irrespective of baseline cytopenias; grade 3-4 diarrhea ~5%, with diarrhea the most common non-hematologic toxicity.
Phase 2 study (Komrokji 2015, Blood) — grade 1/2 diarrhea ~69% and nausea ~49%, establishing GI toxicity as the dominant adverse effect and the driver of volume/electrolyte loss.
FAERS disproportionality analysis (Zhang 2025, Front Oncol) — real-world post-marketing signal with gastrointestinal disorders as the leading system-organ-class and diarrhea the top reported term.

Clinical pearls

The kidney injury is a downstream, functional consequence of pacritinib's dominant toxicity — diarrhea — not intrinsic nephrotoxicity; treat the gut and the volume/electrolyte deficit and the creatinine follows.
Mind the QT-electrolyte loop: pacritinib prolongs the QT interval, and diarrhea-induced hypokalemia and hypomagnesemia amplify that risk — replete potassium and magnesium aggressively and check an ECG.
Diarrhea is usually early (first weeks) and self-limited/manageable — pre-emptive loperamide and hydration prevent most prerenal events, so counsel patients before they start.
Pacritinib's niche is myelofibrosis with severe thrombocytopenia (platelets <50 x 10^9/L) where ruxolitinib/fedratinib cannot be safely dosed; expect thrombocytopenia and anemia as on-target effects, with diarrhea as the manageable GI/renal-relevant toxicity.
A FENa/urine-electrolyte check helps triage: a prerenal signature supports volume repletion over an expensive hunt for intrinsic renal disease.

§05

References

7 primary references — trials, cohorts, mechanism, and reviews. Single-patient case reports are listed separately below, graded by strength. Citation metadata via PubMed / NLM.

Evidence accrual

7 references · 2015–2025 · 2 since 2023

Primary (non–case-report) references per year — a proxy for how actively the agent's renal literature is accruing. Recent years are highlighted. Reflects curation depth, not a systematic bibliometric count.

FDA label — boxed warning & renal dosing· renal impairment

Quoted verbatim from this agent's current FDA label (Jul 2026) — not paraphrased or interpreted. Full label on DailyMed .

Renal impairment — from the label

Avoid use in patients with eGFR <30 mL/min ( 8.7 ).

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 2,964 of them for this agent. Nobody counts the patients who were fine, so none of these numbers is an incidence, a risk, or a rate: they describe what gets reported, shaped by a drug's fame, its indication, and who was watching. How these numbers work.

Reporting odds ratio (ROR) — is kidney injury named in this agent's reports more often than in every other drug's? Above 1 means yes, disproportionately.
Renal phenotypes — the same question asked separately for each kind of kidney injury, so the ratios differ from the overall one and from each other.
Outcomes — a share of this agent's own reports, not of patients: how many were filed as involving a death or a hospitalization. Not a case-fatality rate.

FAERS reported renal phenotypes· 1 signal

Only significant signals appear (95% CI lower bound above 1) — a phenotype missing here was tested and did not reach significance, except Prerenal / Hemodynamic AKI, Pseudo-AKI, Renal Cysts, Chronic Interstitial Nephropathy — outside the clinician-reviewed MedDRA term map, never queried — and ATN and AIN, queried but biopsy-bound: real cases are filed as generic “acute kidney injury”, so their absence is not a negative. As of 2026-08-21.

What reporting says about this profile's documented lesions

Prerenal / Hemodynamic AKINot queried in FAERS — No MedDRA term set is defined for this phenotype, so FAERS was never asked about it.
Electrolyte DisturbanceNo disproportionate reporting — This phenotype IS reportable and this agent has enough reports, yet the reporting is not disproportionate — the one genuinely informative negative of the four.
Acute Tubular NecrosisNot measurable in reporting — Reporters cannot reliably name this lesion, so its absence from FAERS is expected and is not evidence against the documented injury.

Crystal / Obstructive Nephropathy

ROR 1.9195% CI 1.15–3.17· 15 reports

FAERS outcomes & reporting trend· 11.4% of reports w/ death · 18.4% w/ hospitalization

11.4%

Reported with a death outcome

339 of 2,964 reports

18.4%

Reported with hospitalization

546 of 2,964 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 9 systems · 2,964 reports

Bars rank systems by summed reaction-term mentions (a report counts once per term it names) — an ordinal “more vs less reported” cue, not a tally of distinct reports. Renal & urinary first. As of 2026-08-08.

Disproportionality (acute kidney injury):ROR 0.3295% CI 0.15–0.68· 7 AKI reports ·AKI is reported less often than for other drugs (CI entirely below 1) — no disproportionate signal.

Gastrointestinal

Diarrhoea622Nausea290Vomiting93Constipation92Abdominal Discomfort71

General / constitutional

Fatigue381Asthenia151Pain81Malaise80Peripheral Swelling79

Blood & lymphatic

Platelet Count Decreased290Haemoglobin Decreased206Platelet Count Increased61

Nervous system

Dizziness115Headache78

Respiratory

Dyspnoea85

Metabolic & electrolyte

Decreased Appetite78

Immune / infection

Pneumonia74

Skin

Pruritus72

Psychiatric

Insomnia60

Guidelines & consensus· 12

Each recommendation below is this atlas's faithful summary of the source, not a quotation from it — follow the PubMed link for the wording the society published. Summaries may be superseded; consult the current full text and individualize to the patient.

General onco-nephrology references

ADQIThe nephrotoxic effects of anti-cancer therapies: consensus report of the 34th Acute Disease Quality Initiative workgroupNat Rev Nephrol 2026 · PMID 41361704Provides expert-based statements (modified Delphi) on preventing and managing cisplatin/platinum-associated AKI, including isotonic IV hydration, attention to volume status and concomitant nephrotoxins, and incorporates evidence that IV magnesium supplementation may reduce cisplatin-associated AKI; emphasizes risk stratification and standardized AKI definitions.SIRMSIRM-SIN-AIOM: appropriateness criteria for evaluation and prevention of renal damage in the patient undergoing contrast medium examinations-consensus statements from Italian College of Radiology (SIRM), Italian College of Nephrology (SIN) and Italian Association of Medical Oncology (AIOM)Radiol Med 2022 · PMID 35303246Recommends eGFR-based renal risk assessment and pre/post-contrast isotonic saline or sodium bicarbonate hydration; advises maintaining a 5-7 day interval between iodinated contrast administration and cisplatin in cancer patients to reduce additive nephrotoxicity.KDIGOKDIGO Controversies Conference on onco-nephrology: understanding kidney impairment and solid-organ malignancies, and managing kidney cancerKidney Int 2020 · PMID 33126977Identifies platinum compounds (especially cisplatin) as leading cytotoxic causes of acute tubular injury, AKI, and electrolyte/magnesium wasting; calls for interdisciplinary onco-nephrology care, accurate GFR estimation, and individualized drug dosing in patients with reduced kidney function.KDIGOKDIGO Controversies Conference on onco-nephrology: kidney disease in hematological malignancies and the burden of cancer after kidney transplantationKidney Int 2020 · PMID 33276867Addresses chemotherapy-associated AKI/CKD in hematologic cancer, GFR estimation and chemotherapy dosing in patients with reduced kidney function, and management priorities and research gaps for onco-nephrology care.ADDIKDIntegrating International Consensus Guidelines for Anticancer Drug Dosing in Kidney Dysfunction (ADDIKD) into everyday practiceEClinicalMedicine 2025 · PMID 40290844Provides GRADE-based, drug-specific dose-adjustment recommendations for anticancer agents in kidney dysfunction (illustrated for methotrexate, cisplatin, carboplatin and nivolumab); the recommendations build on Part 1's standardised CKD-EPI eGFR assessment rather than Cockcroft-Gault creatinine clearance.ADDIKDAligning kidney function assessment in patients with cancer to global practices in internal medicineEClinicalMedicine 2025 · PMID 40290845Three consensus recommendations: assess kidney function by GFR (measured GFR or CKD-EPI eGFR), classify it using KDIGO categories, and use this uniform approach to dose anticancer drugs — moving cancer medicine away from Cockcroft-Gault estimated creatinine clearance.ADDIKDA methodology for determining dosing recommendations for anticancer drugs in patients with reduced kidney functionEClinicalMedicine 2025 · PMID 40290846Establishes that, where RCT evidence is lacking, anticancer drug dosing recommendations in kidney dysfunction should be derived by critically appraising observational literature via GRADE combined with structured international multidisciplinary consensus voting.KDIGODiagnosis, evaluation, and management of acute kidney injury: a KDIGO summary (Part 1)Crit Care 2013 · PMID 23394211Defines/stages AKI by serum creatinine and urine output; emphasizes avoiding nephrotoxins, maintaining euvolemia/perfusion, dose-adjusting drugs to kidney function, and monitoring high-risk patients — the framework applied to nephrotoxic anti-cancer agents.KDIGOExecutive summary of the KDIGO 2021 Guideline for the Management of Glomerular DiseasesKidney Int 2021 · PMID 34556300Provides the staging/treatment framework for drug-associated glomerular lesions (e.g., bisphosphonate- and interferon-related collapsing FSGS, VEGF-inhibitor podocytopathy/proteinuria), including immunosuppression and supportive RAAS-blockade strategies.KDIGOExecutive summary of the KDIGO 2024 Clinical Practice Guideline for the Management of ANCA-Associated VasculitisKidney Int 2024 · PMID 38388147Updates immunosuppressive induction (rituximab/cyclophosphamide), incorporates avacopan and lower-dose or glucocorticoid-sparing regimens — the management framework for drug- and checkpoint-inhibitor-associated ANCA/pauci-immune glomerulonephritis.KDIGOExecutive summary of the KDIGO 2024 Clinical Practice Guideline for the Management of Lupus NephritisKidney Int 2024 · PMID 38182299Updates first-line lupus nephritis therapy to combination immunosuppression with the addition of belimumab or a calcineurin inhibitor (voclosporin) — informs management of immune-complex/lupus-like glomerulonephritis encountered with immunotherapy.KDIGOExecutive summary of the KDIGO 2025 Clinical Practice Guideline for the Management of Immunoglobulin A Nephropathy (IgAN) and Immunoglobulin A Vasculitis (IgAV)Kidney Int 2025 · PMID 40975525Encourages liberal kidney biopsy and stricter proteinuria control (<0.5 g/d, ideally <0.3 g/d) with RAAS blockers, SGLT2 inhibitors, and targeted-release budesonide — the framework for IgA-dominant glomerular lesions, including those triggered by immune-modulating cancer therapy.

Where Pacritinib sits in nephrotoxicity space — each dot is an anti-cancer agent, positioned so neighbors share a kidney-injury phenotype. Its 6 closest are filled and lead to a numbered marker, matching the numbered cards below.

Position is a 2-D projection (MDS) of each agent's injury signature, nephron target, severity, and class, so two dots can sit close on the page while differing on an axis the projection flattened — the numbered ranking is computed from the full metric, not from the distance you see. Open the full map.

Phenotype-similar agents· the numbered markers on the map above

Alpelisib

Piqray · PI3Kα inhibitor

Profile

Severe hyperglycemia (on-target) → osmotic diuresis and prerenal AKI risk.

PRELYTEATN

Moderate#1 · 89% phenotype match

Lifileucel

Amtagvi · Tumor-infiltrating lymphocyte (TIL) therapy

Profile

2024 cellular therapy; high-dose IL-2 conditioning → capillary leak AKI.

PREATNLYTE

Moderate#2 · 77% phenotype match

Avutometinib

Avmapki (co-packaged with defactinib as Avmapki Fakzynja) · RAF/MEK inhibitor

Profile

RAF/MEK clamp; CK elevation/rhabdomyolysis and tubular electrolyte wasting.

LYTEATNPRE

Moderate#3 · 77% phenotype match

Neratinib

Nerlynx · HER2 / pan-EGFR TKI

Profile

Severe diarrhea → prerenal AKI; loperamide prophylaxis.

PRELYTE

Moderate#4 · 73% phenotype match

Mobocertinib

Exkivity · EGFR exon20 TKI

Profile

Diarrhea-driven prerenal AKI; QT prolongation.

PREATNLYTE

Mild#5 · 72% phenotype match

Arsenic trioxide

Trisenox · Differentiating agent

Profile

Differentiation syndrome; QT prolongation.

PREATNLYTE

Moderate#6 · 71% phenotype match

Compare Pacritinib with its nearest agents

Nearest agents by kidney-injury phenotype (shared injuries, nephron target, severity, class) — a similarity approximation, not a claim of shared drug identity or mechanism.

Kidney risk across Other kinase inhibitors

Same-class agents ordered by their documented kidney-injury profile — atlas severity, an acute-kidney-injury FAERS signal, and how many injury types each is documented to cause. Agents nearer the top carry the lighter documented renal profile.

A comparison of documented kidney-injury data within one drug class — not a substitution recommendation. Efficacy, indication, and non-renal toxicity differ between these agents and are out of scope here. Educational only, not medical advice.