Asciminib hydrochloride, a kinase inhibitor, is an antineoplastic agent.1
Philadelphia Chromosome-Positive Chronic Myeloid Leukemia
Asciminib is used for the treatment of newly diagnosed Philadelphia chromosome-positive chronic myeloid leukemia (Ph+ CML) in adults in the chronic phase of the disease.1, 6 This indication is approved under accelerated approval based on major molecular response (MMR) rate.1 Continued approval for this indication may be contingent upon verification of clinical benefit in a confirmatory trial(s).1
Asciminib is also used for previously treated Ph+ CML in adults in the chronic phase of the disease.1, 2, 5
Efficacy of asciminib for the treatment of newly diagnosed patients with chronic phase Ph+ CML was established based on a phase 3, multicenter, randomized, open-label, active-controlled study (ASC4FIRST) in 405 patients receiving either asciminib 80 mg once daily or an investigator-selected tyrosine kinase inhibitor (TKI).1, 6 The administered TKI (imatinib, nilotinib, dasatinib, or bosutinib) was selected prior to randomization based on patient characteristics and comorbidities.1, 6 A total of 201 patients were randomized to asciminib and 204 patients to investigator-selected TKIs in a 1:1 ratio.6 The primary endpoint was MMR at week 48 and was evaluated for two comparisons: asciminib versus all investigator-selected TKIs and asciminib versus imatinib.1, 6 The median age of patients was 51 years; 37% were female, 54% were white, 44% were Asian, and 1% were Black or African American.1 Of the patients administered TKIs, 99 received imatinib, 49 nilotinib, 42 dasatinib, and 11 bosutinib.1
The median treatment duration was 16.1 months in patients receiving asciminib, 12.9 months with imatinib, and 16.4 months with second-generation TKIs.6 The median follow-up was 16.3 months in the asciminib group and 15.7 months in the investigator-selected TKI group.6 At week 48, MMR occurred in 67.7% of patients in the asciminib group compared to 49% in the investigator-selected TKI group and in 69.3% of patients in the asciminib group compared to 40.2% in the imatinib group.1, 6 The median time to MMR was 24.3 weeks with asciminib and 36.4 weeks with investigator-selected TKIs.6
Efficacy of asciminib for previously treated patients with chronic phase Ph+ CML was established based on a phase 3, multicenter, randomized, open-label, active-controlled study (ASCEMBL) in 233 patients receiving either asciminib 40 mg twice daily or bosutinib 500 mg once daily.1, 2 For inclusion in the study, patients had to have chronic phase Ph+ CML and be treated previously with 2 or more TKIs.1, 2 Patients were stratified to treatment in a 2:1 ratio at randomization based on their major cytogenetic response (MCyR).1, 2 A total of 157 patients were randomized to asciminib and 76 patients were randomized to bosutinib; treatment was continued until unacceptable toxicity or failure occurred.1, 2 The median age of patients was 52 years; 52% were female, 81% were white, and 81% or 18% of patients had an Eastern Cooperative Oncology Group (ECOG) performance status of 0 or 1, respectively.1 Of the participants in the study, 48%, 31%, 15%, and 6% of patients had previously received 2, 3, 4, or 5 or greater prior lines of TKIs, respectively.1
The median treatment duration was 67 weeks in patients receiving asciminib and 30 weeks in patients receiving bosutinib.1 Superiority was demonstrated with asciminib versus bosutinib for the primary endpoint, MMR rate at 24 weeks, which was 25% and 13%, in the respective treatment groups.1, 2 Major molecular response was defined as a breast cancer resistance ABL1 transcript level on the international scale ( BCR-ABL1 IS) of ≤0.1%.1 Asciminib treatment was associated with a higher complete cytogenetic response (CCyR) rate at 24 weeks than bosutinib (41% versus 24%).1 The definition of CCyR was 0% of Ph+ metaphases in bone marrow aspirate with at least 20 examined.1 At 48 weeks, the MMR rate with asciminib was 29% and the MMR rate with bosutinib was 13%.1 A median duration of response had not yet been reached for patients with MMR at any time point after a median duration of follow-up in the study of 20 months.1
Longer term efficacy results (median follow-up of 2.3 years) from ASCEMBL continue to demonstrate the superiority of asciminib over bosutinib.5 The MMR rate at week 96 was 37.6% with asciminib compared to 15.8% with bosutinib.5 In addition, fewer patients experienced treatment failure by the cutoff date with asciminib (51%) than bosutinib (82.9%); median time to treatment failure was also extended with asciminib (24 versus 6 months).5 The estimated 2-year progression-free survival rate was 94.4% with asciminib and 91.1% with bosutinib.5 Similar 2-year estimated overall survival rates were noted with asciminib and bosutinib (97.3% and 98.6%, respectively).5
Guidelines recommend bosutinib, dasatinib, imatinib, or nilotinib for the first-line treatment of newly diagnosed chronic phase CML; selection of the TKI should be based on risk score, toxicity profile, patient's age, ability to tolerate therapy, and presence of comorbid conditions.30 All of these TKIs are appropriate first-line options for patients with chronic phase CML across all risk scores.30 In patients with an intermediate- or high-risk score, disease progression to accelerated or blast phase CML occurs more frequently; bosutinib, dasatinib, and nilotinib are associated with a reduced risk of disease progression than imatinib and are preferred for patients with an intermediate- or high-risk score.30
Asciminib is a second-line treatment option in the guidelines; guidelines were published prior to the approval of asciminib for newly diagnosed patients with chronic phase Ph+ CML.30
Philadelphia Chromosome-Positive Chronic Myeloid Leukemia with T315I Mutation
Asciminib also is used for the treatment of chronic phase Ph+ CML in adults with the T315I mutation.1, 3
Efficacy of asciminib for this use was established based on a phase 1, open-label, randomized study (CABL001X2101) in 45 patients receiving asciminib 200 mg twice daily.1, 3 For inclusion in the study, patients were required to have chronic phase CML with the T315I mutation and to have taken at least 1 TKI previously if no other effective therapy was available.3 Presence of the T315I mutation was confirmed using a qualitative p210 BCR-ABL mutation test with Sanger Sequencing.1 Treatment was continued with asciminib until unacceptable toxicity or treatment failure occurred.1 Of the 45 patients enrolled in the study, 80% were male, and the median age was 54 years.1 Almost half of patients were white (47%), 27% were Asian, and 2.2% were Black or African American.1 The majority of patients (73%) had an ECOG performance status of 0, while the remainder (27%) had a score of 1.1 Those previously receiving 1, 2, 3, 4, and 5 or more TKIs before study entry were 18%, 31%, 36%, 13%, and 2.2% of patients, respectively.1
The primary outcome measure was evaluated in terms of the MMR, defined as BCR-ABL1 IS≤0.1% at 24 and 96 weeks.1, 3 Treatment with asciminib therapy was found to improve MMR in 42% and 49% of patients by 24 and 96 weeks, respectively.1 In patients who had received 2 or fewer previous TKIs, 33% achieved MMR by 6 months; in those who received more than 2 previous TKIs, 10% achieved MMR by 6 months.3 Overall, the median treatment duration with asciminib was 108 weeks.1 In patients with chronic phase CML with the T315I mutation, CCyR was achieved in 41% of patients.3
Ponatinib is generally considered the drug of choice in patients with CML and the T315I mutation.36 While both ponatinib and asciminib have demonstrable activity against the T315I mutation, the drugs have not been compared in clinical trials.4 Based on currently available data, specific clinical scenarios may exist where one drug may be favored over the other.4
Administer asciminib hydrochloride orally.1 Swallow tablets whole.1 Do not break, crush, or chew the tablets.1
Take asciminib without food.1 Avoid food for at least 2 hours before and 1 hour after taking asciminib.1
Missed dose in patients taking once daily regimens: If a dose of asciminib is missed by more than 12 hours, skip the dose and take the next dose as scheduled.1
Missed dose in patients taking twice daily regimens: If a dose is missed by more than 6 hours, skip the dose and take the next dose as scheduled.1
Store asciminib tablets between 20-25°C (excursions permitted between 15-30°C).1 Store in original container to protect the drug from moisture.1
Dosage of asciminib hydrochloride is expressed in terms of asciminib.1
Newly Diagnosed or Previously Treated Chronic Phase Ph+ CML
For the treatment of newly diagnosed or previously treated chronic phase Ph+ CML, the recommended adult dosage of asciminib is 80 mg orally once daily without food taken at approximately the same time each day or 40 mg twice daily administered at approximately 12-hour intervals.1 Continue treatment with asciminib as long as clinical benefit is observed or until unacceptable toxicity occurs.1
Chronic Phase Ph+ CML in Patients with the T315I Mutation
For the treatment of chronic phase Ph+ CML in patients with the T315I mutation, the recommended adult dosage of asciminib is 200 mg orally twice daily without food taken at approximately 12-hour intervals.1
Dosage Modifications for Adverse Reactions
If adverse reactions occur during asciminib therapy, dosage reduction, interruption, and/or permanent discontinuance of the drug may be necessary.1 For recommended dosage reductions for adverse events, see Table 1, and for recommended interventions for specific adverse events see Table 2.1
Dosage Reduction | Dosage for Newly Diagnosed or Previously Treated Chronic Phase Ph+ CML | Dosage for Chronic Phase CML in Patients with T315I mutation |
|---|---|---|
First | 40 mg once daily OR 20 mg twice daily | 160 mg twice daily |
Subsequent | Permanently discontinue asciminib in patients unable to tolerate 40 mg once daily OR 20 mg twice daily | Permanently discontinue asciminib in patients unable to tolerate 160 mg twice daily |
Adverse Reaction | Dosage Modification |
|---|---|
Thrombocytopenia and/or neutropenia | |
Absolute neutrophil count (ANC) <1,000/mm3 and/or platelet count <50,000/mm3 | Withhold drug until ANC resolves to ≥1,000/mm3 and/or platelet count ≥50,000/mm3 If resolved within 2 weeks, resume asciminib at starting dosage If resolved after more than 2 weeks, resume asciminib at reduced dosage For severe, recurrent thrombocytopenia and/or neutropenia, withhold asciminib until ANC recovers to ≥1,000/mm3 and platelet count ≥50,000/mm3, then resume at reduced dosage |
Asymptomatic amylase and/or lipase elevation | |
Elevation>2 × upper limit of normal (ULN) | Withhold drug until resolves to <1.5 × ULN If resolved, resume asciminib at a reduced dosa if events reoccur at the reduced dosage, permanently discontinue therapy If not resolved, permanently discontinue asciminib; perform diagnostic workup to exclude pancreatitis |
Non-hematologic adverse reactions | |
Grade 3a or higher | Withhold drug until recovery to grade ≤1 If resolved, resume asciminib at reduced dosage If not resolved, permanently discontinue asciminib |
aBased on Common Terminology Criteria for Adverse Events (CTCAE) v 4.03.
No dosage adjustment is necessary in patients with mild (total bilirubin at or below upper limit of normal [ULN] and AST above ULN or total bilirubin >1-1.5 times ULN and any AST) to severe hepatic impairment (total bilirubin above 3 times ULN and any AST).1
No dosage adjustment is necessary in patients with mild to severe renal impairment (estimated glomerular filtration rate [eGFR] 15-89 mL/min per 1.73 m2) and not requiring dialysis.1
The manufacturer makes no specific dosage recommendations for geriatric patients.1
Thrombocytopenia, neutropenia, and anemia can occur in patients receiving asciminib.1 Thrombocytopenia occurred in 156 of 556 (28%) patients receiving asciminib; grade 3 or 4 thrombocytopenia was reported in 39 (7%) and 53 (10%) patients, respectively.1 In those with grade 3 or 4 thrombocytopenia, the median time to first occurrence was 6 weeks (range 0.1-64 weeks).1 Of the patients with thrombocytopenia, 11 (2%) patients permanently discontinued asciminib, while the drug was temporarily withheld in 70 (13%) patients.1
Neutropenia occurred in 120 (22%) patients receiving asciminib; grade 3 and 4 neutropenia was reported in 41 (7%) and 35 (6%) patients, respectively.1 Among the patients with grade 3 or 4 neutropenia, the median time to first occurrence was 7 weeks (range 0.1-180 weeks).1 Of the patients with neutropenia, 7 (1.3%) patients permanently discontinued asciminib, while the drug was temporarily withheld in 52 (9%) patients due to the adverse reaction.1
Anemia occurred in 70 (13%) patients receiving asciminib; grade 3 anemia occurred in 22 (4%) patients.1 Of the patients with grade 3 or 4 anemia, the median time to first occurrence was 22 weeks (range 0.1-207 weeks).1 Of the patients with anemia, asciminib was temporarily withheld in 2 (0.4%) patients due to the adverse reaction.1
Perform complete blood count (CBC) every two weeks for the first 3 months of treatment and monthly thereafter or as clinically indicated.1 Monitor patients for signs and symptoms of myelosuppression.1
Based on the severity of thrombocytopenia and/or neutropenia, reduce dose, temporarily withhold, or permanently discontinue asciminib.1
In patients receiving asciminib, pancreatitis occurred in 11 of 556 (2%) patients, with grade 3 pancreatitis occurring in 6 (1.1%) patients.1 Of the patients with pancreatitis, 3 (0.5%) patients permanently discontinued asciminib, while the drug was temporarily withheld in 6 (1.1%) patients due to the adverse reaction.1 Elevation of serum lipase and amylase occurred in 107 (19%) patients receiving asciminib; grade 3 and grade 4 pancreatic enzyme elevations occurred in 41 (7%) and 11 (2%) patients, respectively.1 Of the patients with elevated pancreatic enzymes, asciminib was permanently discontinued in 11 (2%) patients.1
Assess serum lipase and amylase levels monthly during treatment with asciminib, or as clinically indicated.1 Monitor patients for signs and symptoms of pancreatic toxicity.1 Perform more frequent monitoring in patients with a history of pancreatitis.1 If lipase and amylase elevations are accompanied by abdominal symptoms, temporarily withhold asciminib and consider appropriate diagnostic tests to exclude pancreatitis.1
Based on the severity of lipase and amylase elevation, reduce dose, temporarily withhold, or permanently discontinue asciminib.1
Hypertension occurred in 90 of 556 (16%) patients receiving asciminib, with grade 3 or 4 hypertension reported in 49 (9%) and 1 (0.2%) patients, respectively.1 The median time to first occurrence in patients with grade 3 or 4 hypertension was 32 weeks (range, 0.1 to 365 weeks).1 Of the patients with hypertension, asciminib was temporarily withheld in 5 (0.9%) patients due to the adverse reaction.1
Monitor and manage hypertension using standard antihypertensive therapy during treatment with asciminib as clinically indicated; for grade 3 or higher hypertension, temporarily withhold, reduce dose, or permanently discontinue asciminib depending on the persistence of hypertension.1
Hypersensitivity occurred in 168 of 556 (30%) patients receiving asciminib, with grade 3 or 4 hypersensitivity reported in 7 (1.3%) patients, including reactions such as rash, edema, and bronchospasm.1 Monitor patients for signs and symptoms of hypersensitivity and initiate appropriate treatment as clinically indicated; for grade 3 or higher hypersensitivity reactions, temporarily withhold, reduce dose, or permanently discontinue asciminib depending on hypersensitivity persistence.1
Cardiovascular toxicity (including ischemic cardiac and CNS conditions, arterial thrombotic and embolic conditions) and cardiac failure occurred in 60 (11%) and 13 (2.3%) of 556 patients receiving asciminib, respectively.1 Grade 3 cardiovascular toxicity was reported in 14 (2.5%) patients, while grade 3 cardiac failure was observed in 5 (0.9%) patients.1 Grade 4 cardiovascular toxicity occurred in 4 (0.7%) patients, with fatalities occurring in 4 (0.7%) patients.1 Grade 4 cardiac failure was reported in 1 (0.2%) patient; this patient passed.1 Asciminib was permanently discontinued in 4 (0.7%) patients due to cardiovascular toxicity and in 1 (0.2%) patient due to cardiac failure.1 In most patients, cardiovascular toxicity occurred in patients with pre-existing cardiovascular conditions or risk factors, and/or prior exposure to multiple TKIs.1
Arrhythmia, including QTc prolongation, occurred in 35 (6%) patients receiving asciminib, with grade 3 or 4 arrhythmia reported in 10 (1.8%) and 2 (0.4%) patients, respectively.1 Prolongation of the QTc occurred in 5 (0.9%) patients receiving asciminib, with grade 3 QTc prolongation reported in 2 (0.4%) patients.1
Monitor patients with a history of cardiovascular risk factors for cardiovascular signs and symptoms.1 Initiate appropriate treatment as clinically indicated; for grade 3 or higher cardiovascular toxicity, temporarily withhold, reduce dose, or permanently discontinue asciminib depending on cardiovascular toxicity persistence.1
Fetal/Neonatal Morbidity and Mortality
Based on findings from animal studies and its mechanism of action, asciminib can cause fetal harm when administered to a pregnant woman.1 In animal reproduction studies, administration of asciminib to pregnant rats and rabbits during the period of organogenesis caused adverse developmental outcomes including embryo-fetal mortality and malformations at maternal exposures equivalent to or less than those in patients at the recommended doses.1
Verify the pregnancy status of females of reproductive potential before starting treatment with asciminib.1
Based on animal studies and the mechanism of action, asciminib can cause embryo-fetal harm when administered to a pregnant woman.1 There are no available data on the use of asciminib in pregnant women to evaluate a drug-associated risk.1 Animal reproduction studies demonstrated that oral administration of asciminib during organogenesis induced structural abnormalities, embryo-fetal mortality, and alterations to growth.1 Advise patients of the potential risk to a fetus.1
There are no data on the presence of asciminib or its metabolites in human milk, the effects on the breastfed child, or milk production.1
Because of the potential for serious adverse reactions in the breastfed child, advise women not to breastfeed during treatment with asciminib and for 1 week after the last dose.1
Females and Males of Reproductive Potential
Based on findings from animal studies, asciminib can cause embryo-fetal harm when administered to a pregnant woman.1
Verify the pregnancy status of females of reproductive potential before starting treatment with asciminib.1
Females of reproductive potential should use effective contraception during treatment with asciminib and for 1 week after the last dose.1
Based on findings in animals, asciminib may impair fertility in females of reproductive potential.1 The reversibility of the effect on fertility is unknown.1
The safety and efficacy of asciminib in pediatric patients have not been established.1
Of the 556 patients administered asciminib in the ASC4FIRST, ASCEMBL, and X2101 studies, 130 (23%) were ≥65 years of age and 31 (6%) were ≥75 years of age.1
Overall, no differences in safety or efficacy of asciminib were observed between patients ≥65 years of age compared to younger patients.1
Changes in exposure to asciminib in patients with hepatic impairment are not considered clinically meaningful.1 No dosage adjustment is required for patients with mild (total bilirubin at or below ULN and AST above ULN or total bilirubin above 1-1.5 times ULN and any AST) to severe (total bilirubin above 3 times ULN and any AST) hepatic impairment.1
Changes in exposure to asciminib in patients with renal impairment are not considered clinically meaningful.1 No dosage adjustment is required for patients with mild to severe renal impairment (eGFR 15-89 mL/min/1.73 m2) and not requiring dialysis.1
The most common adverse reactions (≥20%) reported with asciminib are musculoskeletal pain, rash, fatigue, upper respiratory tract infections, headache, abdominal pain, and diarrhea.1
The most common select laboratory abnormalities (≥20%) reported with asciminib are decreased lymphocyte, leukocyte, platelet, and neutrophil counts, decreased corrected calcium, increased lipase, increased cholesterol, increased uric acid, increased alanine aminotransferase, increased alkaline phosphatase, decreased hemoglobin, increased triglycerides, increased creatine kinase, increased amylase, and increased aspartate aminotransferase.1
Asciminib is metabolized principally by cytochrome P-450 (CYP) isoenzyme 3A4 (CYP3A4) and UDP-glucuronosyltransferase (UGT) isoenzymes 2B7 (UGT2B7) and UGT2B17.1 The drug is eliminated by biliary secretion via breast-cancer resistance protein (BCRP).1
Asciminib is a substrate of CYP3A4, BCRP, and P-glycoprotein (P-gp), and is an inhibitor of CYP3A4, CYP2C9, P-gp, BCRP, organic anion transporter polypeptides (OATP)1B1 and OATP1B3, and organic cation transporter (OCT)1.1
Drugs Affecting or Affected by Hepatic Microsomal Enzymes
Concomitant use of strong CYP3A4 inhibitors increases the peak plasma concentration (Cmax) and AUC of asciminib.1 Closely monitor for adverse reactions during concomitant use of asciminib at 200 mg twice daily.1
The effects of concomitant use of asciminib with strong CYP3A inducers have not been fully characterized.1
Concomitant use of asciminib with CYP3A4 substrates increases the Cmax and AUC of the CYP3A4 substrate, which may increase the risk of adverse reactions of the substrate.1 Closely monitor for adverse reactions during concomitant use of asciminib at 80 mg total daily dose with certain CYP3A4 substrates where minimal concentration changes may lead to serious adverse reactions.1 Avoid the use of asciminib at 200 mg twice daily with certain CYP3A4 substrates where minimal concentration changes may lead to serious adverse reactions.1
Concomitant use of asciminib with CYP2C9 substrates increases the Cmax and AUC of the CYP2C9 substrate, which may increase the risk of adverse reactions of the substrate.1 Avoid concomitant use of asciminib at all recommended doses with CYP2C9 substrates where minimal concentration changes may lead to serious adverse reactions.1 If concomitant use is unavoidable with asciminib at a total daily dose of 80 mg, reduce the CYP2C9 substrate dosage as recommended in its prescribing information.1 If concomitant use is unavoidable with asciminib 200 mg twice daily, consider alternative therapy with a non-CYP2C9 substrate.1
Concomitant use of asciminib and P-gp substrates can increase the plasma concentration of the P-gp substrate.1 Closely monitor for adverse reactions during concomitant use of asciminib at all recommended dosages where minimal concentration changes of the P-gp substrate may lead to serious toxicities.1
Concomitant use of asciminib may increase the Cmax and AUC of OATP1B and BCRP substrates, which may increase the risk of adverse effects of these substrates.1 Avoid coadministration of asciminib at all recommended doses with rosuvastatin and atorvastatin.1 Closely monitor for adverse effects in patients treated with asciminib with concomitant OATP1B or BCRP substrates.1 Reduce the dosage of the other OATP1B or BCRP substrates as recommended in their prescribing information when used with asciminib.1
Itraconazole Oral Solution Containing Hydroxylpropyl--Cyclodextrin
Concomitant use of itraconazole oral solution containing hydroxypropyl-β-cyclodextrin decreases the Cmax and AUC of asciminib, which can decrease efficacy.1 Avoid concomitant use of asciminib at all recommended doses with itraconazole oral solution containing hydroxypropyl-β-cyclodextrin.1 Concomitant use of oral products containing hydroxypropyl-β-cyclodextrin with asciminib other than itraconazole oral solution has not been fully characterized.1
Asciminib is an ABL/BCR-ABL1 tyrosine kinase inhibitor.1 Asciminib inhibits the ABL1 kinase activity of the BCR-ABL1 fusion protein by binding to the ABL myristoyl pocket.1 In studies conducted in vitro or animal models of CML, asciminib showed activity against wild-type BCR-ABL1 and several mutant forms of the kinase, including the T315I mutation.1
Following oral administration, peak plasma concentrations of asciminib are attained at a median of 2.5 hours (range 2-3 hours).1 Asciminib exhibits slightly greater than dose-proportional pharmacokinetics at steady state across the dose range of 10-200 mg administered once or twice daily.1 Administration with a high-fat meal decreases the Cmax and AUC of asciminib by 68% and 62%, respectively, and administration with a low-fat meal decreases the Cmax and AUC of asciminib by 35% and 30%, respectively.1 Asciminib is 97% bound to human plasma proteins.1 The half-life of asciminib is 5.5 hours at a dosage of 40 mg twice daily or 80 mg once daily, and 9 hours at 200 mg twice daily.1 Following oral administration of a single radio-labeled dose of asciminib, 80% (57% unchanged) and 11% (2.5% unchanged) of the dose were recovered in the feces and urine of healthy subjects, respectively.1 No clinically significant differences in the pharmacokinetics of asciminib have been observed based on sex, age (range 20-88 years), race, or body weight (range 42-184 kg).1
Additional Information
The American Society of Health-System Pharmacists, Inc. represents that the information provided in the accompanying monograph was formulated with a reasonable standard of care, and in conformity with professional standards in the field. Readers are advised that decisions regarding use of drugs are complex medical decisions requiring the independent, informed decision of an appropriate health care professional, and that the information contained in the monograph is provided for informational purposes only. The manufacturer's labeling should be consulted for more detailed information. The American Society of Health-System Pharmacists, Inc. does not endorse or recommend the use of any drug. The information contained in the monograph is not a substitute for medical care. For further information on the handling of antineoplastic agents, see the ASHP Guidelines on Handling Hazardous Drugs at [Web].
Excipients in commercially available drug preparations may have clinically important effects in some individuals; consult specific product labeling for details.
Please refer to the ASHP Drug Shortages Resource Center for information on shortages of one or more of these preparations.
Routes | Dosage Forms | Strengths | Brand Names | Manufacturer |
|---|---|---|---|---|
Oral | Tablets, film-coated | 20 mg (of asciminib) | Scemblix® | Novartis |
40 mg (of asciminib) | Scemblix® | Novartis | ||
100 mg (of asciminib) | Scemblix® |
AHFS® Drug Information. © Copyright, 1959-2026, Selected Revisions May 10, 2025. American Society of Health-System Pharmacists, Inc., 4500 East-West Highway, Suite 900, Bethesda, MD 20814.
1. Novartis Pharmaceuticals Corporation. SCEMBLIX® (asciminib) tablets prescribing information. East Hanover, NJ; 2024 Oct [Web]
2. Réa D, Mauro MJ, Boquimpani C, et al. A phase 3, open-label, randomized study of asciminib, a STAMP inhibitor, vs bosutinib in CML after 2 or more prior TKIs. Blood . 2021;138(21):2031-2041. [PubMed 34407542]
3. Hughes TP, Mauro MJ, Cortes JE, et al. Asciminib in Chronic Myeloid Leukemia after ABL Kinase Inhibitor Failure. N Engl J Med . 2019;381(24):2315-2326. [PubMed 31826340]
4. Shanmuganathan N, Hughes TP. Asciminib for chronic myeloid leukaemia: Next questions [published online ahead of print, 2022 Jun 21]. Br J Haematol . 2022;10.1111/bjh.18323. [PubMed 35729850]
5. Hochhaus A, Rea D, Boquimpani C, et al. Asciminib vs bosutinib in chronic-phase chronic myeloid leukemia previously treated with at least two tyrosine kinase inhibitors: longer-term follow-up of ASCEMBL. Leukemia . 2023;37:617-26.
6. Hochhaus A, Wang J, Kim DW, et al. Asciminib in newly diagnosed chronic myeloid leukemia. N Engl J Med . 2024;391:885-98.
30. Shah NP, Bhatia R, Altman JK, et al. Chronic myeloid leukemia, Version 2.2024. J Natl Compr Cancer Netw . 2024;22(1):43-69.
36. Hochhaus A, Saussele S, Rosti G, et al. Chronic myeloid leukaemia: ESMO Clinical Practice Guidelines for diagnosis, treatment and follow-up. Ann Oncol. 2018;29(Suppl 4):iv261. [PubMed 30285223]