How should kidney function be monitored during Olverembatinib therapy?

Baseline and periodic urinalysis / urine albumin-to-creatinine ratio; Blood pressure at each visit; Creatine phosphokinase (CPK) — interpret as muscle, not kidney; Tumor lysis labs (urate, K, phosphate, calcium) at initiation in high-burden disease.

How can kidney injury from Olverembatinib be prevented?

Optimize blood pressure before and during therapy

Who is at higher risk of kidney injury from Olverembatinib?

Pre-existing hypertension or chronic kidney disease; Pre-existing proteinuria; Prior or concurrent VEGF-pathway inhibitor exposure; Heavily pretreated patients (prior ponatinib/asciminib) with cumulative vascular risk; Volume depletion or concurrent nephrotoxins.

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Printable monograph

BCR-ABL1 tyrosine kinase inhibitor (3rd generation)

Olverembatinib

Olverembatinib (HQP1351) · BCR-ABL TKI

BCR-ABL1 tyrosine kinase inhibitor (3rd generation) · approved 2021 · 5 citations

Up to date· through 2026

Thinly sourced3/9 · 3 signals

Not met: 5 citations
Not met: 12+ references
Not met: Accrued over 10+ years (span: 4y)
Met: Beyond single case reports
Not met: Peer-reviewed sources
Met: Landmark reference
Met: Current through 2026
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.

Potent T315I-active TKI with a largely renal-sparing profile

Mild2021 China approval; global phase 3 (POLARIS) program ongoing 2023-2026

Chronic-phase CML with the T315I mutation after prior TKI therapyAccelerated-phase CML with the T315I mutationChronic-phase CML resistant or intolerant to first- and second-generation TKIsInvestigational: Ph+ ALL, succinate-dehydrogenase-deficient GIST (POLARIS program)

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Signature kidney injury

Signature lesion

Glomerular Injury / Proteinuria

Renal-specific data are sparse. In the Chinese phase 1/2 program (n=165) proteinuria was among the common treatment-related adverse events, though grade and exact rate were not separately quantified; clinically significant AKI was not a prominent signal. Direct nephrotoxicity appears low overall.Source: Proteinuria listed among common treatment-related AEs in the phase 1/2 trial (Jiang Q et al., J Hematol Oncol 2022; PMID 35982483).

Onset & rechallenge

Time to injuryVariable / unpredictable

Onset is variable, with proteinuria and hypertension from multi-kinase TKIs typically emerging over weeks to months of therapy.

Distilled from: “Variable; proteinuria and hypertension, when they occur with multi-kinase TKIs, typically emerge over weeks to months of therapy.”

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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.

Glomerular Injury / Proteinuria#1 · Signatureno population incidence denominator
Proteinuria is listed among the common treatment-related adverse events in the pivotal phase 1/2 program (165 TKI-resistant CML patients); podocyte/glomerular proteinuria is the characteristic renal signal of this third-generation BCR-ABL1 TKI (no population incidence denominator reported). PMID 35982483 (opens PubMed in a new tab)
HypertensionSecondaryqualitative — no citable incidence
Raised blood pressure — archetypally on-target loss of endothelial nitric oxide from VEGF-pathway blockade, studied as a pharmacodynamic marker of drug exposure. Other agents raise it too: vascular effects of BCR-ABL, BTK and RET inhibitors and of copanlisib; abiraterone's mineralocorticoid excess; androgen suppression or blockade.
Prerenal / Hemodynamic AKISecondaryqualitative — no citable incidence
Renal hypoperfusion from capillary leak and cytokine storm — IL-2 and CAR-T cytokine release syndrome.
Pseudo-AKISecondaryqualitative — no citable incidence
The great mimic — a rise in creatinine from blocked tubular secretion (OCT2/MATE), NOT true injury. The GFR is intact; confirm with cystatin C before stopping effective therapy.

Toxicity fingerprint

Tap a signature to trace where it strikes the nephron.

Incidence not quantified

SeverityMild

ReversibilityVariable

Evidence5 citations

Nephron map

GlomerulusFiltration barrier (podocytes + endothelium)

Vasculature / Endothelium

Proximal Tubule

Glomerular Injury / Proteinuria

Damage to the filtration barrier — podocyte injury, FSGS and protein leak from VEGF and mTOR blockade.

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Kidney injury

Mechanism of kidney injury

No direct tubulotoxic mechanism is established. The plausible renal signature is glomerular/podocyte injury and VEGF-pathway-type effects (proteinuria, hypertension) shared with multi-kinase BCR-ABL TKIs such as ponatinib, arising from off-target inhibition of VEGFR/PDGFR signaling important to glomerular endothelial-podocyte homeostasis. A critical interpretive caveat: the most frequent laboratory abnormality is elevated blood creatine phosphokinase (CPK) — a skeletal-muscle marker, not a kidney marker — which must not be misread as renal injury, though severe CPK rise raises a theoretical pigment/rhabdomyolysis concern. Any small creatinine rise in the absence of true GFR loss could also reflect transporter-mediated (pseudo-AKI) effects, but this is inferred from class rather than proven for olverembatinib.

Clinical presentation

Most patients have no clinically apparent kidney disease. When present, the renal footprint is low-grade proteinuria, occasionally with treatment-emergent hypertension. Frank AKI, nephrotic-range proteinuria, or electrolyte wasting were not characteristic in registrational data. Elevated CPK (often asymptomatic, sometimes with myalgia) is common and is a muscular, not renal, finding.

Management

For low-grade proteinuria, monitor with serial UACR and manage blood pressure (RAAS blockade where appropriate); dose interruption/reduction is reserved for worsening or nephrotic-range proteinuria, mirroring ponatinib-class practice. Treat treatment-emergent hypertension per standard guidelines. Marked CPK elevation should prompt evaluation for myopathy/rhabdomyolysis rather than being treated as primary kidney injury; ensure adequate hydration if pigment nephropathy is a concern. There is no agent-specific renal antidote; supportive care and hematology/nephrology co-management apply.Lesion-level management framework

Risk factors

Pre-existing hypertension or chronic kidney disease
Pre-existing proteinuria
Prior or concurrent VEGF-pathway inhibitor exposure
Heavily pretreated patients (prior ponatinib/asciminib) with cumulative vascular risk
Volume depletion or concurrent nephrotoxins

Prevention

Optimize blood pressure before and during therapy

Anticancer mechanism· how it treats cancer

Orally bioavailable third-generation BCR-ABL1 tyrosine kinase inhibitor that potently inhibits native BCR-ABL1 and a broad spectrum of resistance mutants, including the gatekeeper T315I mutation and compound mutations. It binds the ATP pocket of the ABL1 kinase domain, halting constitutive kinase signaling that drives Philadelphia-chromosome-positive CML and ALL. Like ponatinib, it has multi-kinase activity (including against VEGFR/PDGFR-family and KIT), which underlies both its broad efficacy and its off-target vascular and podocyte-relevant effects.

Note · No dedicated nephrotoxicity study of olverembatinib exists as of mid-2026; this profile reasons conservatively from registrational safety data and BCR-ABL/multi-kinase TKI class behavior.

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Clinical depth

Renal dose adjustment

Standard dosing is 30-40 mg orally every other day (30 mg for non-T315I per the phase 1b recommended dose; 40 mg the RP2D in the Chinese program). No validated renal-impairment dose adjustment has been published; pharmacokinetics support alternate-day dosing, and a high-fat meal substantially increases exposure (Cmax +106%, AUC +70%), so administration relative to food should be consistent. Use clinical caution in significant renal impairment given limited data.

Dialyzability & ESKD dosing

Not appreciably dialyzable (no formal data). As a small-molecule TKI that is highly protein-bound and lipophilic with a large apparent volume of distribution, it is unlikely to be appreciably removed by hemodialysis.

Differential diagnosis

Distinguish drug-related glomerular proteinuria from CML-related or unrelated causes (diabetic/hypertensive nephropathy, paraproteins). Critically, separate an isolated CPK rise (skeletal-muscle origin, very common with olverembatinib) from true renal injury. Consider prerenal/hemodynamic AKI from volume depletion or concurrent nephrotoxins, and TLS-related urate nephropathy in high-burden disease at initiation.

Monitoring

Baseline and periodic urinalysis / urine albumin-to-creatinine ratio
Blood pressure at each visit
Creatine phosphokinase (CPK) — interpret as muscle, not kidney
Tumor lysis labs (urate, K, phosphate, calcium) at initiation in high-burden disease

Key trials & series

Phase 1/2 China registrational program in T315I and TKI-resistant CML (NCT03883087, NCT03883100; Jiang Q et al., J Hematol Oncol 2022, PMID 35982483)
Phase 1b global bridging RCT after >=2 TKIs including ponatinib/asciminib failure (NCT04260022; Jabbour E et al., JAMA Oncol 2025, PMID 39570620)
POLARIS-1/-2/-3 phase 3 registrational program (NCT06051409, NCT06423911, NCT06640361)

Clinical pearls

The dominant lab abnormality is elevated CPK (~39% all-grade in the global phase 1b) — a muscle marker, NOT a sign of kidney injury; do not confuse it with creatinine.
Proteinuria is the recurring renal signal, consistent with VEGF/multi-kinase class effects shared with ponatinib.
Direct nephrotoxicity and frank AKI were not prominent in registrational data — treat the renal profile as largely sparing but monitor proteinuria and blood pressure.
A high-fat meal markedly increases exposure (AUC +70%); keep food timing consistent to avoid swings that could amplify off-target effects.

Beyond the kidney — non-renal toxicities· 3 organ systems

Class-level context for the major non-renal toxicities of the BCR-ABL1 tyrosine kinase inhibitor (3rd generation) class.

Vascular

Hypertension, VTE/ATE, bleeding, aneurysm

Vascular occlusion (ponatinib), fluid retention

Pulmonary

Pneumonitis, ILD, effusions, hypertension

Pleural effusions (dasatinib), PAH

Cardiac

Cardiomyopathy, QT, ischemia, myocarditis

QT, heart failure

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References

4 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

4 references · 2022–2026 · 3 since 2024

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.

Case reports — ranked by strength· 1

Single-patient and small-series reports, graded by evidentiary strength — A Strong (biopsy-proven plus a series and/or positive rechallenge), B Moderate, and C Limited (a single clinically-diagnosed case). Strongest first. Grades are inferred automatically from each report's abstract and journal — a heuristic ranking aid, not a formal quality appraisal.

CaseB · ModerateOlverembatinib and high-dose methotrexate in acute lymphoblastic leukemia: delayed methotrexate clearance and increased nephrotoxicity.Tian JX et al. · Leuk Lymphoma 2026 · PMID 41739441Small series of 10 olverembatinib-treated ALL patients showing the drug markedly slows methotrexate clearance, causing a 60% rate of grade >=2 nephrotoxicity and 70% acute kidney injury.

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 Olverembatinib 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

Adagrasib

Krazati · KRAS G12C inhibitor

Profile

Creatinine rise; emerging data.

PREGLOMPSEUDO

Mild#1 · 66% phenotype match

Asciminib

Scemblix · BCR-ABL STAMP inhibitor

Profile

Hypertension and pancreatitis; allosteric BCR-ABL inhibitor.

HTNPRE

Mild#2 · 65% phenotype match

Sunitinib

Sutent · VEGFR TKI

Profile

VEGFR-TKI; hypertension and proteinuria, TMA reported.

HTNGLOMTMA

Moderate#3 · 63% phenotype match

Naxitamab

Danyelza · Anti-GD2 antibody

Profile

Anti-GD2 antibody; infusion-related hypertension and prerenal AKI.

PREHTN

Moderate#4 · 59% phenotype match

Brigatinib

Alunbrig · ALK TKI

Profile

Creatinine elevation; usually benign.

PSEUDOPREHTN

Mild#5 · 59% phenotype match

Lorlatinib

Lorbrena · ALK TKI

Profile

Edema and metabolic effects.

PSEUDOPREGLOM

Mild#6 · 59% phenotype match

Compare Olverembatinib 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 BCR-ABL 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.

1NilotinibPRE — Prerenal / Hemodynamic AKIMild
2AsciminibHTN — HypertensionMild
3BosutinibPSEUDO — Pseudo-AKIMild
4ImatinibLYTE — Electrolyte DisturbanceMild
5Olverembatinib· this agentGLOM — Glomerular Injury / ProteinuriaMild
6PonatinibHTN — HypertensionModerate
7DasatinibGLOM — Glomerular Injury / ProteinuriaFAERS AKIModerate

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.