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Printable monograph

IDH1 inhibitor

Ivosidenib

Tibsovo · Ivo

IDH1 inhibitor · approved 2018 · 6 citations

Recent· through 2024
Fairly sourced5/9 · 5 signals
  • Met: 6 citations
  • Not met: 12+ references
  • Not met: Accrued over 10+ years (span: 6y)
  • Met: Beyond single case reports
  • Met: High-impact journal
  • Met: Landmark reference
  • Met: Current through 2024
  • 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.

An IDH1 inhibitor whose kidney risk is indirect — differentiation syndrome and tumor lysis driving AKI.

ModerateIDH1 inhibitor
IDH1-mutant acute myeloid leukemiaIDH1-mutant cholangiocarcinoma
§01

Signature kidney injury

Differentiation (IDH) syndrome is a recognized, potentially fatal complication — reported in roughly 10-19% of AML patients across IDH-inhibitor experience (e.g. ~10.4-11.7% with the IDH2 inhibitor enasidenib in pooled/phase 1-2 analyses) — and can drive AKI through capillary leak, fluid overload, hypotension, and inflammation; tumor lysis can also occur with cytoreduction.Source: DiNardo et al., N Engl J Med 2018

Onset & rechallenge

Time to injurySubacute (~1–6 weeks)

Tumor lysis is early during cytoreduction; differentiation syndrome runs days to weeks (median ~30 days).

Distilled from: “Differentiation syndrome typically days to weeks after starting therapy (median ~30 days); tumor lysis early during cytoreduction.”

§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.

  1. Prerenal / Hemodynamic AKI#1 · Signatureno population incidence denominator

    IDH1-inhibitor differentiation syndrome (capillary leak, fluid overload -> prerenal/hemodynamic AKI) occurred as a grade >=3 treatment-related event in 3.9% of relapsed/refractory AML patients on ivosidenib. PMID 29860938 (opens PubMed in a new tab)

  2. 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).

  3. Acute Tubular NecrosisRarequalitative — 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
ReversibilityVariable
Evidence6 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

Kidney injury is largely indirect. Differentiation syndrome — driven by a cytokine surge from rapidly differentiating myeloblasts — causes systemic inflammation, capillary leak, hemodynamic instability, and fluid overload that produce a prerenal/hemodynamic AKI (sometimes with concurrent ATN). Tumor lysis syndrome from rapid blast clearance adds uric acid and phosphate load with crystal/electrolyte-mediated AKI.

Clinical presentation

Differentiation syndrome: dyspnea/hypoxia, fever, peripheral edema, pulmonary infiltrates, weight gain, hypotension, and rising creatinine, often with leukocytosis; median onset ~30 days (range days to ~4 months). Tumor lysis: hyperuricemia, hyperphosphatemia, hyperkalemia, hypocalcemia, and AKI. QT prolongation is a separate class effect.

Management

Prompt systemic corticosteroids (e.g. dexamethasone ~10 mg IV q12h) and supportive care for differentiation syndrome, with diuresis for fluid overload, leukapheresis/hydroxyurea for marked leukocytosis, and drug interruption if severe or unresponsive; TLS management with aggressive hydration, rasburicase or allopurinol, electrolyte correction, and renal replacement therapy if refractory.Lesion-level management framework

Risk factors

  • High leukemic/blast burden and high LDH
  • Rapid response/cytoreduction
  • Baseline renal impairment
  • Volume-overload states

Prevention

  • Vigilance for differentiation syndrome from the first weeks
  • TLS prophylaxis (IV hydration, urate-lowering therapy)
Anticancer mechanism· how it treats cancer

Inhibits mutant isocitrate dehydrogenase-1 (IDH1), lowering the oncometabolite 2-hydroxyglutarate and inducing myeloid differentiation. Approved for IDH1-mutant acute myeloid leukemia and IDH1-mutant cholangiocarcinoma.

Note · Kidney injury is predominantly secondary to differentiation syndrome and tumor lysis rather than direct tubular toxicity. IDH2-inhibitor (enasidenib) data are used as class-informative context for differentiation-syndrome incidence and management.
§04

Clinical depth

Renal dose adjustment

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.

Dialyzability & ESKD dosing

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.

Differential diagnosis

IDH differentiation-syndrome AKI (capillary leak, fluid overload, hypotension, leukocytosis, pulmonary infiltrates) vs tumor-lysis AKI (hyperuricemia/hyperphosphatemia/hyperkalemia) vs sepsis or nephrotoxin-related ATN in a neutropenic leukemia patient. The two on-target syndromes frequently overlap and can coexist.

Monitoring

  • Daily clinical assessment for differentiation syndrome (dyspnea, edema, weight, oxygenation, WBC) during the first weeks
  • Electrolytes, uric acid, phosphate, calcium, and creatinine for tumor lysis during cytoreduction
  • ECG/QTc (QT prolongation is a recognized class effect)

Key trials & series

  • AG120-C-001 (registrational ivosidenib in relapsed/refractory IDH1-mutant AML — DiNardo NEJM 2018)
  • Roboz 2020 frontline IDH1-mutant AML cohort
  • Fathi 2018 / Montesinos 2024 IDH-inhibitor differentiation-syndrome analyses (enasidenib, class-informative)

Clinical pearls

  • The kidney is an innocent bystander: AKI here is driven by differentiation syndrome and tumor lysis, not direct tubular toxicity.
  • Start corticosteroids early and do not necessarily stop the drug — most differentiation syndrome is managed without permanent discontinuation.
  • Layer TLS prophylaxis (hydration plus urate-lowering) at initiation in high-burden disease, and watch for the two syndromes overlapping.
Beyond the kidney — non-renal toxicities· 2 organ systems

Class-level context for the major non-renal toxicities of the IDH1 inhibitor class.

Pulmonary

Pneumonitis, ILD, effusions, hypertension

  • Differentiation syndrome

Cardiac

Cardiomyopathy, QT, ischemia, myocarditis

  • QT prolongation
§05

References

6 primary references — trials, cohorts, mechanism, and reviews. Citation metadata via PubMed / NLM.

Evidence accrual

6 references · 2018–2024 · 1 since 2022
202018: 2 citations2020: 2 citations2021: 1 citation2024: 1 citation201820202024

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.

  1. 1.LandmarkDurable Remissions with Ivosidenib in IDH1-Mutated Relapsed or Refractory AML.DiNardo CD et al. · N Engl J Med · 2018 · PMID 29860938Pivotal trial describing IDH differentiation syndrome and leukocytosis as key on-target safety events.
  2. 2.Ivosidenib induces deep durable remissions in patients with newly diagnosed IDH1-mutant acute myeloid leukemia.Roboz GJ et al. · Blood · 2020 · PMID 31841594Frontline AML data reporting differentiation syndrome among notable adverse events.
  3. 3.Differentiation syndrome with lower-intensity treatments for acute myeloid leukemia.Fathi AT et al. · Am J Hematol · 2021 · PMID 33625753Expert review of IDH/FLT3-inhibitor differentiation syndrome, including AKI, diagnostic criteria, and corticosteroid management.
  4. 4.Differentiation Syndrome Associated With Enasidenib, a Selective Inhibitor of Mutant Isocitrate Dehydrogenase 2: Analysis of a Phase 1/2 Study.Fathi AT et al. · JAMA Oncol · 2018 · PMID 29346478Characterizes IDH-inhibitor differentiation syndrome (~12%), median onset 30 days, and corticosteroid-based management — class-informative for ivosidenib.
  5. 5.Differentiation syndrome associated with treatment with IDH2 inhibitor enasidenib: pooled analysis from clinical trials.Montesinos P et al. · Blood Adv · 2024 · PMID 38507688Pooled analysis quantifying IDH-inhibitor differentiation-syndrome incidence (~10.4%), risk factors, and management across trials.
  6. 6.Ivosidenib in IDH1-mutant, chemotherapy-refractory cholangiocarcinoma (ClarIDHy): a multicentre, randomised, double-blind, placebo-controlled, phase 3 study.Abou-Alfa GK et al. · Lancet Oncol · 2020 · PMID 32416072Pivotal ClarIDHy trial extending ivosidenib to IDH1-mutant cholangiocarcinoma; registrational safety dataset.
FDA label — boxed warning & renal dosing· boxed warning · renal impairment

Quoted verbatim from this agent's current FDA label (Dec 2025) — not paraphrased or interpreted. Full label on DailyMed .

Boxed warning

WARNING: DIFFERENTIATION SYNDROME IN AML AND MDS Patients treated with TIBSOVO have experienced symptoms of differentiation syndrome, which can be fatal. Symptoms may include fever, dyspnea, hypoxia, pulmonary infiltrates, pleural or pericardial effusions, rapid weight gain or peripheral edema, hypotension, and hepatic, renal, or multi-organ dysfunction. If differentiation syndrome is suspected, initiate corticosteroid therapy and hemodynamic monitoring until symptom resolution [see Warnings and Precautions (5.1) and Adverse Reactions (6.1) ] . WARNING: DIFFERENTIATION SYNDROME IN AML AND MDS See full prescribing information for complete boxed warning. Patients treated with TIBSOVO have experienced symptoms of differentiation syndrome, which can be fatal. If differentiation syndrome is suspected, initiate corticosteroid therapy and hemodynamic monitoring until symptom resolution ( 5.1 , 6.1 ).

Renal impairment — from the label

No modification of the starting dose is recommended for patients with mild or moderate renal impairment (eGFR ≥ 30 mL/min/1.73m 2 , MDRD). The pharmacokinetics and safety of ivosidenib in patients with severe renal impairment (eGFR < 30 mL/min/1.73m 2 , MDRD) or renal impairment requiring dialysis are unknown [see Clinical Pharmacology (12.3) ] . For patients with pre-existing severe renal impairment or who are requiring dialysis, consider the risks and potential benefits before initiating treatment with TIBSOVO.

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 2,057 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 2026-10-01.

What reporting says about this profile's documented lesions

  • Electrolyte Disturbancecorroborated · ROR 1.61 — but the naming terms alone are not disproportionate, so this rests on terms merely consistent with the lesion
  • Prerenal / Hemodynamic AKINot queried in FAERS — No MedDRA term set is defined for this phenotype, so FAERS was never asked about it.
  • 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.
Electrolyte Disturbance
ROR 1.6195% CI 1.12–2.31· 30 reports
FAERS outcomes & reporting trend· 10.1% of reports w/ death · 31.2% w/ hospitalization
10.1%

Reported with a death outcome

207 of 2,057 reports

31.2%

Reported with hospitalization

642 of 2,057 reports

Reports per year

  • 2015: 0 reports
  • 2016: 0 reports
  • 2017: 4 reports
  • 2018: 23 reports
  • 2019: 236 reports
  • 2020: 431 reports
  • 2021: 398 reports
  • 2022: 99 reports
  • 2023: 176 reports
  • 2024: 175 reports
  • 2025: 290 reports
  • 2026: 225 reports

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 8 systems · 2,057 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 2026-10-01.

Disproportionality (acute kidney injury):ROR 1.0095% CI 0.60–1.67· 15 AKI reports ·no disproportionate AKI reporting signal (CI spans 1).
Gastrointestinal
Nausea121Diarrhoea119Vomiting65Constipation41
Blood & lymphatic
Febrile Neutropenia74Platelet Count Decreased74Neutropenia65Thrombocytopenia57Haemoglobin Decreased53
General / constitutional
Fatigue169Pyrexia62Asthenia59
Immune / infection
Pneumonia59Infection52
Nervous system
Headache45Dizziness41
Cardiac
Electrocardiogram Qt Prolonged76
Respiratory
Dyspnoea58
Musculoskeletal
Arthralgia42
Guidelines & consensus· 13

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 2024 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease: known knowns and known unknownsKidney Int 2024 · PMID 38519239Evaluate and risk-stratify CKD, manage to delay progression and its complications, and practise explicit medication management and drug stewardship — the framework the atlas's G1–G5 eGFR banding and every renal dose-adjustment recommendation sit inside. Because the guideline excludes dialysis and transplant recipients by its own statement of scope, its recommendations do not carry to those settings, where this atlas's dialyzability and post-transplant guidance rests on other sources.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 Ivosidenib 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.

1. Arsenic trioxide12. Enasidenib23. Gallium nitrate34. Lifileucel45. Tretinoin (ATRA)56. Tagraxofusp6Ivosidenib
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

Arsenic trioxide

Trisenox · Differentiating agent

Profile

Differentiation syndrome; QT prolongation.

PREATNLYTE
Moderate#1 · 100% phenotype match

Enasidenib

Idhifa · IDH2 inhibitor

Profile

Differentiation syndrome and tumor lysis.

PREATNLYTE
Moderate#2 · 100% phenotype match

Gallium nitrate

Ganite · Antineoplastic metal salt

Profile

Dose-limiting acute tubular necrosis; potentiated by dehydration and concurrent nephrotoxins.

ATNPRELYTE
Moderate#3 · 88% phenotype match

Lifileucel

Amtagvi · Tumor-infiltrating lymphocyte (TIL) therapy

Profile

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

PREATNLYTE
Moderate#4 · 85% phenotype match

Tretinoin (ATRA)

Vesanoid · Retinoid (differentiating agent)

Profile

Differentiation syndrome → capillary leak and AKI.

PREATN
Moderate#5 · 84% phenotype match

Tagraxofusp

Elzonris · IL-3 immunotoxin

Profile

Capillary-leak syndrome → AKI.

PREATN
Moderate#6 · 84% phenotype match
Compare Ivosidenib 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 targeted agents

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.

  1. 1BelzutifanMild
  2. 2CasdatifanMild
  3. 3DordaviproneMild
  4. 4IberdomideMild
  5. 5RucaparibMild
  6. 6SonidegibMild
  7. 7TalazoparibMild
  8. 8GlasdegibMild
  9. 9ImetelstatMild
  10. 10NiraparibMild
  11. 11NirogacestatMild
  12. 12OlaparibMild
  13. 13RelacorilantMild
  14. 14SotorasibMild
  15. 15TazemetostatMild
  16. 16VismodegibMild
  17. 17VorasidenibMild
  18. 18PomalidomideMild
  19. 19ThalidomideMild
  20. 20AdagrasibFAERS AKIMild
  21. 21Denileukin diftitoxModerate
  22. 22Afamitresgene autoleucel (Afami-cel)Moderate
  23. 23OlutasidenibModerate
  24. 24ZiftomenibModerate
  25. 25EnasidenibModerate
  26. 26Gallium nitrateModerate
  27. 27Ivosidenib· this agentModerate
  28. 28LenalidomideModerate
  29. 29RevumenibModerate
  30. 30IxazomibFAERS AKIModerate
  31. 31BortezomibFAERS AKIModerate
  32. 32TagraxofuspFAERS AKIModerate
  33. 33Tretinoin (ATRA)FAERS AKIModerate
  34. 34Arsenic trioxideFAERS AKIModerate
  35. 35LifileucelFAERS AKIModerate
  36. 36SelinexorFAERS AKIModerate
  37. 37Moxetumomab pasudotoxSevere
  38. 38SonrotoclaxSevere
  39. 39CarfilzomibFAERS AKISevere
  40. 40VenetoclaxFAERS AKISevere

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.