Adagrasib, an irreversible inhibitor of Kirsten rat sarcoma viral oncogene homolog ( KRAS ) G12C, is an antineoplastic agent.1
Adagrasib, as a single agent, is used for the treatment of adult patients with Kirsten rat sarcoma viral oncogene homolog ( KRAS ) G12C-mutated locally advanced or metastatic non-small cell lung cancer (NSCLC), as determined by an FDA approved test, who have received at least one prior systemic therapy.1 The drug has been designated an orphan drug by FDA for use in this condition.2
This indication is approved under accelerated approval based on objective response rate and duration of response.1 Continued approval for this indication may be contingent upon verification and description of a clinical benefit in a confirmatory trial(s).1
Efficacy of adagrasib was evaluated in KRYSTAL-1, a single-arm, open label expansion of a phase I/IB dose-finding trial.1, 3, 4 Patients ≥18 years of age with a confirmed diagnosis of metastatic or unresectable NSCLC with KRAS mutation previously treated with a platinum-based chemotherapy regimen and immune checkpoint inhibitor, with an Eastern Cooperative Oncology Group (ECOG) performance status of 0 or 1, and ≥1 measurable lesion based on Response Evaluation criteria in Solid Tumors (RECIST v 1.1) were eligible for study enrollment.1, 4 Adagrasib was administered at a dosage of 600 mg twice daily in a fasted state until disease progression, study withdrawal, toxicity, or death.1, 4 The primary outcome was objective response; secondary outcomes included disease control (stable, complete, or partial response), duration of response, progression-free survival, overall survival, and 1-year survival rate.1, 4
A total of 112 evaluable patients were included in the efficacy analysis.1 The median age of patients was 64 years; 55% were female, 83% were white, and 83% had an ECOG performance status of 1.1 Adenocarcinoma was present in 97% of patients, and 89% had metastatic disease.1 An objective response was seen in 43% of patients, with 0.9% having a complete response and 42% a partial response.1 Stable disease was seen in 36.6% of patients.4 The median duration of response was 8.5 months; 58% of patients had a duration of response of ≥6 months.1 Disease control was reported in 79.5% of patients; median progression-free survival was 6.5 months with a median overall survival of 12.6 months.4 The 1-year estimated overall survival was 50.8%.4
The American Society of Clinical Oncology (ASCO) and Ontario Health (OH; formerly known as Cancer Care Ontario) 2021 joint guideline specifically addressed treatment of stage IV NSCLC harboring driver alterations, including epidermal growth factor receptor ( EGFR ), b-Raf serine-threonine kinase ( BRAF ) V600E, and proto-oncogene receptor tyrosine kinase ( ROS1 ) mutations.5 The oncogenic KRAS mutation has been reported in 33% of patients with advanced NSCLC, with 13% as KRAS G12C.6 The most recent update from ASCO on advanced NSCLC with driver alterations states that clinicians may offer sotorasib or adagrasib to patients with KRAS G12C as a second-line treatment option after immune checkpoint inhibitor therapy and/or chemotherapy.7 Recommendations from a Canadian group are also available specific to KRAS G12C-mutated advanced NSCLC, with first line treatment as immune checkpoint inhibitors with or without chemotherapy (i.e., platinum doublet).6 For patients progressing on first line therapy, platinum doublet (if not used as part of first line therapy) or sotorasib are preferred.6 Adagrasib is considered an acceptable treatment option.6
Adagrasib, in combination with cetuximab, is used for the treatment of adult patients with KRAS G12-C-mutated locally advanced or metastatic colorectal cancer, as determined by an FDA-approved test, who have received prior therapy with fluoropyrimidine-, oxaliplatin-, and irinotecan-based chemotherapy.1
This indication is approved under accelerated approval based on objective response rate and duration of response.1 Continued approval for this indication may be contingent upon verification and description of a clinical benefit in a confirmatory trial(s).1
Efficacy of adagrasib in combination with cetuximab was evaluated in KRYSTAL-1, a single-arm, open label, expansion cohort study.1 Enrolled patients had a confirmed diagnosis of locally advanced or metastatic KRAS G12-mutated colorectal cancer, an ECOG performance status of 0 or 1, and received appropriate prior therapy (e.g., fluoropyrimidine-, oxaliplatin-, and irinotecan-based chemotherapy and potentially a vascular endothelial growth factor [VEGF] inhibitor).1 Adagrasib was administered at a dosage of 600 mg twice daily in combination with cetuximab given either at a dosage of 500 mg/m2 every 2 weeks or 400 mg/m2 as an initial dose followed by 250 mg/m2 weekly; treatment was continued until unacceptable toxicity or disease progression.1 The major efficacy outcomes were objective response rate and duration of response.1
A total of 94 evaluable patients were included in the efficacy analysis.1 The median age of patients was 57 years; 53% were female, 71% were white, 14% were Black or African American, 5% were Asian, and 1.1% were American Indian or Alaska Native.1 Patients received a median of 3 prior systemic therapies (range, 1 to 9).1 The objective response rate was 34% with all patients experiencing a partial response.1 The median duration of response was 5.8 months; 31% of patients experienced a duration of response ≥6 months.1
Adagrasib is administered orally twice daily when given as a single agent or in combination with cetuximab.1 Administer at the same time every day, with or without food.1
Swallow tablets whole; do not chew, crush, or split the tablets.1
If vomiting occurs after taking a dose of adagrasib, do not take an additional dose; resume dosing at the next scheduled time.1
If a dose of adagrasib is missed, skip the dose if more than 4 hours have elapsed from the expected dosing time; resume dosing at the next scheduled time.1
Store tablets at 20-25ºC (excursions permitted between 15-30ºC).1
The recommended adult dosage of adagrasib is 600 mg orally twice daily; continue treatment until disease progression or unacceptable toxicity occurs.1
The recommended adult dosage of adagrasib in combination with cetuximab is 600 mg orally twice daily; continue treatment until disease progression or unacceptable toxicity occurs.1 Refer to the cetuximab prescribing information for specific dosage information of this agent.1
Dosage Modification for Toxicity
If adverse effects occur during adagrasib therapy, temporary interruption of therapy, dosage reduction, and/or permanent discontinuance of the drug may be necessary.1
Consult Table 1 for recommended dosage reductions for adverse reactions for use of adagrasib as a single agent or in combination with cetuximab.1 If an adverse reaction occurs, a maximum of 2 dosage reductions are allowed; permanently discontinue adagrasib in patients who are unable to tolerate 600 mg once daily.1
Please refer to the cetuximab prescribing information for dose modifications for cetuximab-related adverse reactions.1 If adagrasib is withheld or permanently discontinued, withhold or permanently discontinue cetuximab.1 If cetuximab is permanently discontinued, monotherapy with adagrasib may be continued.1
Dosage Reduction | Recommended Dosage |
|---|---|
First dose reduction | 400 mg twice daily |
Second dose reduction | 600 mg once daily |
Consult Table 2 for recommended dosage adjustments for specific adverse reactions based on severity.1
Adverse Reaction | Severity | Recommended Dosage Adjustment |
|---|---|---|
Nausea or vomiting despite appropriate supportive care, including antiemetic therapy | Grade 3 or 4 | Withhold until recovery to grade 1 or lower or return to baseline; resume at the next lower dosage level |
Diarrhea despite appropriate supportive care, including antidiarrheal therapy | Grade 3 or 4 | Withhold until recovery to grade 1 or lower or return to baseline; resume at the next lower dosage level |
QTc interval prolongation | Absolute QTc value >500 ms OR an increase of >60 ms from baseline | Withhold until QTc interval is <481 ms or returns to baseline; resume at the next lower dosage level |
Torsade de pointes, polymorphic ventricular tachycardia, or signs or symptoms of serious or life-threatening arrhythmia | Permanently discontinue | |
Hepatotoxicity | Grade 2, AST or ALT | Decrease dosage to the next lower dosage level |
Grade 3 or 4, AST or ALT | Withhold until recovery to grade 1 or lower or return to baseline; resume at the next lower dosage level | |
AST or ALT >3 times ULN with total bilirubin >2 times ULN in the absence of alternative causes | Permanently discontinue | |
Interstitial lung disease or pneumonitis | Any grade | Withhold if interstitial lung disease/pneumonitis is suspected; permanently discontinue if confirmed |
Other adverse reactions | Grade 3 or 4 | Withhold until recovery to grade 1 or lower or return to baseline; resume at the next lower dosage level |
ALT, alanine aminotransferase; AST, aspartate aminotransferase; ULN, upper limit of normal.
The manufacturer makes no specific dosage recommendations for patients with hepatic impairment.1
The manufacturer makes no specific dosage recommendations for patients with renal impairment.1
The manufacturer makes no specific dosage recommendations for geriatric patients.1
Severe GI adverse reactions can occur with adagrasib as single-agent therapy.1 Serious reactions have been reported, including GI bleeding (3.8%, including 0.8% with grade 3 or 4 events), GI obstruction (1.6%, including 1.4% with grade 3 or 4 events), colitis (0.5%, including 0.3% with grade 3 events), ileus (0.5%), and stenosis (0.3%).1 In adagrasib clinical trials, nausea, diarrhea, or vomiting occurred in 89% of patients, including 9% with grade 3 events; these reactions led to treatment interruption or dosage reduction in 29% of patients and permanent discontinuation of adagrasib in 0.3% of patients.1
Serious GI adverse reactions may also occur when adagrasib is administered with cetuximab.1 These reactions include GI bleeding (8.5%, including 1.1% with grade 3 or 4 events), GI obstruction (5.3%; all grade 3 or 4 events), colitis (1.1%; all grade 3 events), and ileus (1.1%).1 Nausea, diarrhea, or vomiting was reported in 92% of 94 patients administered combination therapy, with 6% experiencing grade 3 events.1 Dose interruption or dose reduction due to nausea, diarrhea, or vomiting occurred in 23% of patients.1
Monitor for GI adverse reactions during treatment with adagrasib.1 Provide supportive care (including antidiarrheals, antiemetics, or fluid replacement) as indicated.1 Withhold therapy, reduce the dosage, or permanently discontinue adagrasib based on severity of the reaction.1
Adagrasib can cause prolongation of the QT interval corrected for rate (QTc), which can increase the risk for ventricular tachyarrhythmias (e.g., torsades de pointes) or sudden death.1
In patients who had ≥1 postbaseline ECG in the pooled safety population of single agent adagrasib, an average QTc≥501 ms was observed in 6% of patients, and 11% of patients had an increase from baseline of QTc of >60 ms.1 Adagrasib causes concentration-dependent QTc interval increases.1
In those who received adagrasib in combination with cetuximab, 5% of patients with ≥1 postbaseline ECG assessment had an average QTc≥501 ms and 16% had an increase from baseline of >60 ms.1
Avoid adagrasib in patients with congenital long QT syndrome and in those with concurrent QTc prolongation, as well as in patients taking other drugs known to prolong the QTc interval.1
Monitor ECGs and electrolytes, particularly potassium and magnesium, prior to adagrasib initiation, when concomitant use of adagrasib with other drugs known to prolong the QT interval cannot be avoided, and as clinically indicated in patients with congestive heart failure, bradyarrhythmias, or electrolyte abnormalities.1 Electrolyte abnormalities should be corrected.1 Withhold therapy, reduce the dosage, or permanently discontinue adagrasib based on severity of the reaction.1
Adagrasib can cause hepatotoxicity, which may result in drug-induced liver injury and hepatitis.1
In the pooled safety population of single agent adagrasib, drug-induced liver injury was reported in 0.3% of patients, with 0.3% experiencing grade 3 events.1 Increased ALT/AST was observed in 32% of patients, including grade 3 (5%) and grade 4 (0.5%) events.1 The median time to first onset of elevated ALT/AST was 3 weeks (range, 0.1-48 weeks).1 Overall hepatotoxicity occurred in 37% of patients, with grade 3/4 events in 7% of patients; hepatotoxicity led to treatment interruption or dosage reduction in 12% of patients and discontinuation of adagrasib in 0.5% of patients.1
In those who received adagrasib in combination with cetuximab, increased ALT/AST was seen in 29% of patients, including grade 3 (5%) and grade 4 (1.1%) events.1 The median time to initial onset of elevated ALT/AST was 4 weeks (range, 0.1-27 weeks).1 Overall hepatotoxicity occurred in 38% of patients, with grade 3/4 events reported in 10% of patients.1 Adagrasib dose interruption or reduction occurred in 12% of patients.1
Monitor liver function tests (AST, ALT, alkaline phosphatase, and total bilirubin) prior to adagrasib initiation and monthly for 3 months during treatment or as clinically indicated, with more frequent testing in patients who develop transaminase elevations.1 Withhold therapy, reduce the dosage, or permanently discontinue adagrasib based on severity of the reaction.1
Interstitial Lung Disease/Pneumonitis
Interstitial lung disease (ILD)/pneumonitis, including fatal cases, can occur with adagrasib therapy.1
In the pooled safety population of patients who received adagrasib as a single agent, ILD/pneumonitis was reported in 4.1% of patients, including 1.4% of patients with grade 3/4 cases and a fatality.1 The median time to first onset of ILD/pneumonitis was 12 weeks (range, 5-31 weeks).1 Adagrasib was discontinued due to ILD/pneumonitis in 0.8% of patients.1
In those who received adagrasib in combination with cetuximab, grade 1 ILD/pneumonitis was reported in 1.1% of patients.1 The time to initial onset of ILD/pneumonitis was 38 weeks.1
Monitor patients for new or worsening respiratory symptoms indicative of ILD/pneumonitis (e.g., dyspnea, cough, fever) during adagrasib therapy.1 Withhold adagrasib if ILD/pneumonitis is suspected, and permanently discontinue therapy if no other potential causes of ILD/pneumonitis are identified.1
There are no available human data on the use of adagrasib during pregnancy.1 In animal reproduction studies, oral administration of adagrasib to pregnant rats and rabbits during organogenesis did not result in adverse developmental effects or embryofetal lethality at exposures below the human exposure at the recommended dosage of 600 mg twice daily.1
It is unknown whether adagrasib (or its metabolites) is distributed into human milk or if the drug has any effect on milk production or the nursing infant.1
Because of the potential for serious adverse reactions in nursing infants, advise women not to breast-feed during treatment with adagrasib and for 1 week after the last dose.1
Females and Males of Reproductive Potential
Findings from animal studies indicate that adagrasib may impair fertility in females and males of reproductive potential.1
Safety and efficacy of adagrasib have not been established in pediatric patients.1
In the KRYSTAL-1 study evaluating adagrasib in patients with locally advanced or metastatic KRAS G12C-mutated non-small cell lung cancer (NSCLC), 49% of patients who received adagrasib 600 mg orally twice daily were ≥65 years of age and 13% were ≥75 years of age.1 There were no overall differences in adagrasib efficacy or safety between geriatric and younger patients.1
In patients with metastatic colorectal cancer who received adagrasib 600 mg orally twice daily in combination with cetuximab, 33% were ≥65 years of age and 2.1% were ≥75 years of age.1 There were no overall differences in efficacy or safety between geriatric and younger patients with combination therapy.1
No clinically important differences in adagrasib pharmacokinetics are expected in patients with mild to severe hepatic impairment (Child-Pugh classes A to C).1
No clinically important differences in adagrasib pharmacokinetics are expected in patients with mild to severe renal impairment (creatinine clearance 15 to <90 mL/minute).1
The most common adverse reactions (≥25%) in clinical trials of patients with NSCLC receiving adagrasib as a single agent include nausea, diarrhea, vomiting, fatigue, musculoskeletal pain, hepatotoxicity, renal impairment, edema, dyspnea, and decreased appetite.1
The most common grade 3 or 4 laboratory abnormalities (≥2%) include decreased lymphocytes, decreased hemoglobin, increased ALT, increased AST, hypokalemia, hyponatremia, increased lipase, decreased leukocytes, decreased neutrophils, and increased alkaline phosphatase.1
The most common adverse reactions (≥25%) in clinical trials of patients with colorectal cancer receiving adagrasib in combination with cetuximab include rash, nausea, diarrhea, vomiting, fatigue, musculoskeletal pain, hepatotoxicity, headache, dry skin, abdominal pain, decreased appetite, edema, anemia, and cough.1
The most common grade 3 or 4 laboratory abnormalities (≥2%) include decreased lymphocytes, decreased potassium, decreased magnesium, decreased hemoglobin, increased AST, increased lipase, decreased albumin, and increased ALT.1
Adagrasib is a cytochrome P-450 (CYP) isoenzyme 3A4 substrate.1 Adagrasib is an inhibitor of CYP isoenzymes 3A, 2C9, and 2D6, and the efflux transporter P-glycoprotein (P-gp).1
In vitro studies indicate that adagrasib may inhibit CYP isoenzyme 2B6, multidrug and toxin extrusion (MATE)-1, and MATE-2K, and may be a substrate of breast cancer resistance protein (BCRP).1
Drugs Affecting Hepatic Microsomal Enzymes
Concomitant use of adagrasib with a strong CYP3A inducer reduces adagrasib exposure and may consequently reduce effectiveness of the drug.1
Concomitant administration of rifampin, a strong CYP3A inducer, with a single dose of adagrasib 600 mg decreased peak plasma concentration and AUC of adagrasib by 88 and 95%, respectively.1 Concomitant administration of rifampin with multiple doses of adagrasib 600 mg is predicted to decrease the peak plasma concentration and AUC of adagrasib by >61 and >66%, respectively.1
Avoid concomitant use of adagrasib with strong CYP3A inducers.1
Concomitant use of adagrasib with a strong CYP3A inhibitor increases adagrasib concentrations if adagrasib concentrations have not reached steady state; this may increase the risk of adverse reactions from adagrasib.1
Concomitant administration of itraconazole, a strong CYP3A inhibitor, with a single dose of adagrasib 200 mg resulted in 2.4-fold and 4-fold increases in the peak plasma concentration and AUC of adagrasib, respectively.1 No clinically important differences in adagrasib pharmacokinetics at steady state were predicted when used concomitantly with itraconazole.1
Avoid concomitant use of adagrasib with strong CYP3A inhibitors until adagrasib concentrations have reached steady state (after approximately 8 days).1
Drugs Metabolized by Hepatic Microsomal Enzymes
Concomitant use of adagrasib with a sensitive CYP3A substrate increases exposure of the CYP3A substrate and may consequently increase the risk of adverse reactions related to the substrate.1
Concomitant administration of midazolam, a sensitive CYP3A substrate, and adagrasib 400 mg twice daily resulted in 4.8-fold and 21-fold increases in the peak plasma concentration and AUC of midazolam, respectively.1 Concomitant administration of midazolam and adagrasib 600 mg twice daily is predicted to result in 3.1-fold and 31-fold increases in the peak plasma concentration and AUC of midazolam, respectively.1
Avoid concomitant use of adagrasib with sensitive CYP3A substrates unless otherwise recommended in the prescribing information for these substrates.1
Concomitant use of adagrasib with a sensitive CYP2C9 substrate increases exposure of the CYP2C9 substrate and may consequently increase the risk of adverse reactions related to the substrate.1
Concomitant administration of warfarin, a sensitive CYP2C9 substrate, and adagrasib 600 mg twice daily is predicted to result in 1.1-fold and 2.9-fold increases in the peak plasma concentration and AUC of warfarin, respectively.1
Avoid concomitant use of adagrasib with sensitive CYP2C9 substrates where minimal concentration changes may lead to serious adverse reactions, unless otherwise recommended in the prescribing information for these substrates.1
Concomitant use of adagrasib with a sensitive CYP2D6 substrate increases exposure of the CYP2D6 substrate and may consequently increase the risk of adverse reactions related to the substrate.1
Concomitant administration of dextromethorphan, a sensitive CYP2D6 substrate, and adagrasib 400 mg twice daily resulted in 1.9-fold and 1.8-fold increases in the peak plasma concentration and AUC of dextromethorphan, respectively.1 Concomitant administration of dextromethorphan and adagrasib 600 mg twice daily is predicted to result in 1.7-fold and 2.4-fold increases in the peak plasma concentration and AUC of dextromethorphan, respectively.1
Avoid concomitant use of adagrasib with sensitive CYP2D6 substrates where minimal concentration changes may lead to serious adverse reactions, unless otherwise recommended in the prescribing information for these substrates.1
Drugs Affected by the P-glycoprotein Transport System
Concomitant use of adagrasib with a P-gp substrate increases exposure of the P-gp substrate and may consequently increase the risk of adverse reactions related to the substrate.1
Concomitant administration of digoxin, a P-gp substrate, and adagrasib 600 mg twice daily is predicted to result in 1.9-fold and 1.5-fold increases in the peak plasma concentration and AUC of digoxin, respectively.1
Avoid concomitant use of adagrasib with P-gp substrates where minimal concentration changes may lead to serious adverse reactions, unless otherwise recommended in the prescribing information for these substrates.1
Drugs that Prolong the QTc Interval
Concomitant use of adagrasib with other products that prolong the QT interval corrected for rate (QTc) may result in a greater increase in the QTc interval and adverse reactions associated with QTc interval prolongation (e.g., torsade de pointes, other serious arrythmias, sudden death).1
Avoid concomitant use of adagrasib with other drugs known to prolong the QTc interval.1 If concomitant use cannot be avoided, monitor ECG and electrolytes prior to adagrasib initiation, during concomitant use, and as clinically indicated.1 Withhold adagrasib if the QTc interval is >500 or if the change from baseline is >60; refer to Table 2 in the Dosage section for more information.1
No clinically important differences in adagrasib pharmacokinetics were predicted or observed when used concomitantly with efavirenz, a moderate CYP3A inducer.1
No clinically important differences in adagrasib pharmacokinetics were predicted or observed when used concomitantly with pantoprazole, a proton pump inhibitor.1
No clinically important differences in adagrasib pharmacokinetics were predicted or observed when used concomitantly with rosuvastatin, a BCRP/organic anion transporting polypeptide substrate.1
Adagrasib is an irreversible inhibitor of Kirsten rat sarcoma viral oncogene homolog ( KRAS ) G12C and belongs to the RAS GTPase family.1 Adagrasib forms a covalent bond with the mutant cysteine in KRAS G12C, locking the mutant KRAS protein in an inactive state that prevents downstream signaling; wild-type KRAS is not affected.1 In KRAS G12C-mutated tumor xenograft models, adagrasib resulted in tumor regression and displayed minimal off-target activity.1 Combination therapy with adagrasib and cetuximab demonstrated increased antitumor activity in some KRAS G12C-mutant colorectal tumor xenograft models compared to administration of either therapy alone.1
The exposure-response relationships of adagrasib and the time course of pharmacodynamic response are unknown.1 Adagrasib increases the QT interval corrected for rate (QTc) in a concentration-dependent manner.1
Adagrasib peak plasma concentrations and AUC increase proportionally over the dose range of 400-600 mg (0.67-1 times the approved recommended dosage).1 Steady-state is reached within 8 days following administration of the approved recommended dosa accumulation was approximately 6-fold.1 The median time to peak plasma concentration of adagrasib is approximately 6 hours.1 No clinically important differences in adagrasib pharmacokinetics were observed following administration of a high-fat, high-calorie meal (approximately 900-1000 calories, 50% from fat).1 In vitro, human plasma protein binding of adagrasib is approximately 98%.1 Following single-dose administration, adagrasib is primarily metabolized by cytochrome P-450 (CYP) isoenzyme 3A4.1 Following multiple dosing to steady-state, adagrasib inhibits its own CYP3A4 metabolism, permitting CYP isoenzymes 2C8, 1A2, 2B6, 2C9, and 2D6 to contribute to metabolism.1 The terminal half-life of adagrasib is 23 hours.1 Following a single oral dose of radiolabeled adagrasib, approximately 75% of the dose (14% unchanged) was excreted in the feces, and 4.5% of the dose (2% unchanged) was excreted in the urine.1 No clinically important differences in adagrasib pharmacokinetics have been observed based on age (19-89 years), sex, race (white, Black or African American, or Asian), body weight (36-146 kg), Eastern Cooperative Oncology Group performance status (0, 1), tumor type (non-small cell lung cancer or colorectal cancer), or tumor burden.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.
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.
Adagrasib is only available through in-network specialty pharmacies and specialty distributors; visit the manufacturer website ([Web]) for more information on access to adagrasib.2
Routes | Dosage Forms | Strengths | Brand Names | Manufacturer |
|---|---|---|---|---|
Oral | Tablets, film-coated | 200 mg | Krazati® | Mirati Therapeutics |
AHFS® Drug Information. © Copyright, 1959-2026, Selected Revisions February 10, 2025. American Society of Health-System Pharmacists, Inc., 4500 East-West Highway, Suite 900, Bethesda, MD 20814.
Only references cited for selected revisions after 1984 are available electronically.
1. Mirati Therapeutics, Inc. Krazati® (adagrasib) ORAL prescribing information. 2024 Jun. [Web]
2. US Food and Drug Administration. Search orphan drug designations and approvals. From FDA website. [Web]
3. Ou S, Janne P, Leal T, et al. First-in-human phase I/IB dose-finding study of adagrasib (MRTX849) in patients with advance KRASG12C solid tumors (KRYSTAL-1). J Clin Oncol . 2022;40:2530-2538. [PubMed 35167329]
4. Janne P, Riely G, Gadgeel S, et al. Adagrasib in non-small-cell lung cancer harboring a KRASG12C mutation. N Engl J Med . 2022;387:120-131. [PubMed 35658005]
5. Hanna N, Robinson A, Temin S, et al. Therapy for stage IV non-small-cell lung cancer with driver alterations: ASCO and OH (CCO) Joint Guideline update. J Clin Oncol . 2021;39:1040-1091. [PubMed 33591844]
6. Cheema P, Banerji S, Blais N, et al. Canadian consensus recommendations on the management of KRAS G12C-mutated NSCLC. Curr Oncol . 2023;30:6473-6496. [PubMed 37504336]
7. Jaiyesimi IA, Leighl NB, Ismaila A, et al. Therapy for stage IV non-small-cell lung cancer with driver alterations: ASCO living guideline, Version 2023.3 J Clin Oncol . 2024;42:e1-e22.
8. Mirati Therapeutics, Inc. Ordering Krazati® (adagrasib). From Krazati® website for US healthcare professionals. [Web]