Is kidney injury from Asciminib reversible?

Reversible. Typical onset: Hypertension can emerge across treatment; pancreatitis often early..

How should kidney function be monitored during Asciminib therapy?

Blood pressure at baseline and regularly; Serum lipase/amylase periodically and with abdominal symptoms; CBC (cytopenias) per schedule.

How can kidney injury from Asciminib be prevented?

Treat elevated blood pressure proactively Cardiovascular risk-factor optimization Dose interruption for grade 3+ hypertension or pancreatitis per label

Who is at higher risk of kidney injury from Asciminib?

Pre-existing hypertension or cardiovascular disease; Prior TKI vascular toxicity; History of pancreatitis or hypertriglyceridemia; Baseline CKD.

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Printable monograph

BCR-ABL STAMP inhibitor

Asciminib

Scemblix · ASC

BCR-ABL STAMP inhibitor · approved 2021 · 7 citations

Up to date· through 2026

Fairly sourced5/9 · 5 signals

Met: 7 citations
Not met: 12+ references
Not met: Accrued over 10+ years (span: 7y)
Met: Beyond single case reports
Met: High-impact journal
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.

Allosteric (STAMP) BCR-ABL1 inhibitor binding the myristoyl pocket — its renal-relevant signals are hypertension and pancreatitis, not a direct nephropathy.

MildAllosteric TKI era

Chronic-phase chronic myeloid leukemia after >=2 prior tyrosine kinase inhibitorsChronic-phase CML with the T315I mutation

§01

Signature kidney injury

Signature lesion

Hypertension

Representative incidence10.5%

Hypertension and pancreatitis (with amylase/lipase elevations) are recognized toxicities; thrombocytopenia/neutropenia are common. In first-line use (ASC4FIRST), hypertension occurred more frequently with asciminib than comparator TKIs — all-grade 10.5%, grade >=3 5.5%. Asciminib has a cleaner overall profile than prior TKIs, and direct nephrotoxicity is not a defined signal — renal effects are largely hypertension-mediated.Source: Han et al., Blood Res 2026 (PMID 42458108, ASC4FIRST first-line hypertension all-grade 10.5%); Rea et al., Blood 2021 (ASCEMBL); Hughes et al., N Engl J Med 2019

Onset & rechallenge

Time to injuryVariable / unpredictable

Hypertension can emerge at any point across treatment, with pancreatitis tending to be early.

Distilled from: “Hypertension can emerge across treatment; pancreatitis often early.”

§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.

Hypertension#1 · Signatureno population incidence denominator
Grade >=3 adverse reaction with incidence >=5% in ASCEMBL (EMA assessment) PMID 37141403 (opens PubMed in a new tab)
Prerenal / Hemodynamic AKIRarequalitative — no citable incidence
Renal hypoperfusion from capillary leak and cytokine storm — IL-2 and CAR-T cytokine release syndrome.

Toxicity fingerprint

Tap a signature to trace where it strikes the nephron.

10.5%incidence

SeverityMild

ReversibilityReversible

Evidence7 citations

Nephron map

GlomerulusFiltration barrier (podocytes + endothelium)

Vasculature / EndotheliumGlomerular & peritubular capillaries

Hypertension

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.

§03

Kidney injury

Mechanism of kidney injury

Asciminib's renal relevance is principally vascular: treatment-emergent hypertension (a class effect of BCR-ABL inhibitors via endothelial/vascular signaling) raises systemic and glomerular pressure and, if uncontrolled and chronic, can contribute to hypertensive kidney injury. Pancreatitis can cause volume shifts and prerenal physiology in severe cases. There is no characteristic direct tubular or glomerular lesion; cardiovascular/vascular occlusive events are tracked as a class concern.

Clinical presentation

New or worsening hypertension; epigastric pain with elevated lipase/amylase in pancreatitis. Renally, a hypertension-associated creatinine trend rather than an acute structural picture; severe pancreatitis can produce dehydration and prerenal AKI.

Management

Control hypertension with standard antihypertensives and continue cardiovascular risk reduction; this protects the kidney from pressure-mediated injury. Manage pancreatitis supportively (IV fluids, holding drug) and treat any resultant prerenal AKI with volume repletion. Dose-interrupt/reduce for significant toxicity; renal effects are generally reversible with control of BP and pancreatitis.Lesion-level management framework

Risk factors

Pre-existing hypertension or cardiovascular disease
Prior TKI vascular toxicity
History of pancreatitis or hypertriglyceridemia
Baseline CKD

Prevention

Treat elevated blood pressure proactively
Cardiovascular risk-factor optimization
Dose interruption for grade 3+ hypertension or pancreatitis per label

Anticancer mechanism· how it treats cancer

First-in-class allosteric BCR-ABL1 inhibitor that binds the myristoyl pocket (Specifically Targeting the ABL Myristoyl Pocket, STAMP) rather than the ATP site, locking the kinase inactive. This circumvents many ATP-site resistance mutations (including T315I at higher dose) in chronic myeloid leukemia.

Note · The renal link is indirect — chiefly hypertension-mediated, with pancreatitis-related volume shifts in severe cases; there is no characteristic direct asciminib nephropathy.

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Clinical depth

Renal dose adjustment

No dose adjustment required for renal impairment in labeling (renal clearance is minor); use general caution in advanced CKD. Hepatic metabolism predominates.

Dialyzability & ESKD dosing

Highly protein-bound; not expected to be dialyzable. No specific ESKD dosing required given minimal renal clearance.

Differential diagnosis

Distinguish hypertension-mediated renal effects from other TKI vascular toxicity and essential hypertension; separate pancreatitis-driven prerenal AKI from intrinsic causes. The absence of a tubular/glomerular lesion is reassuring.

Monitoring

Blood pressure at baseline and regularly
Serum lipase/amylase periodically and with abdominal symptoms
CBC (cytopenias) per schedule

Key trials & series

ASCEMBL (Rea, Blood 2021) — registrational RCT vs bosutinib quantifying hypertension/pancreatitis
Hughes et al. (NEJM 2019) — first-in-human dose-escalation including T315I activity and toxicity

Clinical pearls

Asciminib's allosteric (myristoyl-pocket/STAMP) mechanism gives a cleaner off-target profile than ATP-site TKIs.
Its renal-relevant signals are hypertension and pancreatitis — manage BP to protect the kidney.
Minimal renal clearance means no renal dose adjustment is needed.
Lipase elevations are often asymptomatic; correlate with symptoms before stopping.

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

Class-level context for the major non-renal toxicities of the BCR-ABL STAMP inhibitor 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

§05

References

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

Evidence accrual

7 references · 2019–2026 · 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.

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 3,174 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

Hypertensioncorroborated · ROR 2.43 — on the terms that name the lesion (ROR 3.33)
Prerenal / Hemodynamic AKINot queried in FAERS — No MedDRA term set is defined for this phenotype, so FAERS was never asked about it.

Hypertension

ROR 2.4395% CI 2.05–2.88· 138 reports

FAERS outcomes & reporting trend· 11.2% of reports w/ death · 18% w/ hospitalization

11.2%

Reported with a death outcome

356 of 3,174 reports

18%

Reported with hospitalization

572 of 3,174 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 8 systems · 3,174 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 1.0495% CI 0.70–1.56· 24 AKI reports ·no disproportionate AKI reporting signal (CI spans 1).

Gastrointestinal

Nausea175Diarrhoea130Vomiting74Pancreatitis72Abdominal Pain66

Blood & lymphatic

Thrombocytopenia158Cytopenia86Platelet Count Decreased81Anaemia62Neutropenia62

General / constitutional

Fatigue252Asthenia76Pain68

Respiratory

Pleural Effusion99Dyspnoea87

Musculoskeletal

Arthralgia98Myalgia80

Nervous system

Headache134

Skin

Rash109

Vascular

Hypertension104

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 Asciminib 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

Ponatinib

Iclusig · BCR-ABL TKI

Profile

Vascular toxicity and hypertension.

HTNPRETMA

Moderate#1 · 76% phenotype match

Nilotinib

Tasigna · BCR-ABL TKI

Profile

eGFR decline over time.

PRE

Mild#2 · 73% phenotype match

Naxitamab

Danyelza · Anti-GD2 antibody

Profile

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

PREHTN

Moderate#3 · 72% phenotype match

Acalabrutinib

Calquence · BTK inhibitor

Profile

Tumor lysis; lower hypertension than ibrutinib.

HTNPREXTAL

Mild#4 · 70% phenotype match

Dinutuximab

Unituxin · Anti-GD2 antibody

Profile

Capillary-leak syndrome, hypertension and severe pain in neuroblastoma.

PREHTNTMA

Moderate#5 · 67% phenotype match

Tisotumab vedotin

Tivdak · Antibody-drug conjugate (tissue factor/MMAE)

Profile

Ocular/bleeding toxicity dominates; renal involvement essentially unreported.

PRE

Mild#6 · 65% phenotype match

Compare Asciminib 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
2Asciminib· this agentHTN — HypertensionMild
3BosutinibPSEUDO — Pseudo-AKIMild
4ImatinibLYTE — Electrolyte DisturbanceMild
5OlverembatinibGLOM — 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.