Capmatinib, a mesenchymal-epithelial transition (MET) tyrosine kinase inhibitor, is an antineoplastic agent.1, 3, 4, 5, 6
Capmatinib is used for the treatment of metastatic non-small cell lung cancer (NSCLC) in adults whose tumors harbor a mesenchymal-epithelial transition ( MET ) exon 14 skipping mutation as detected by an FDA-approved companion diagnostic test.1, 3 Capmatinib has been designated an orphan drug by FDA for use in this condition.2 Information on FDA-approved companion diagnostic tests for the detection of MET mutations in NSCLC is available on FDA's website ([Web]).1 The current indication is based on objective response rate and duration of response; continued approval for this indication may be contingent upon verification and description of clinical benefit in confirmatory studies.1
A relatively small subset of patients with NSCLC have MET exon 14 skipping mutation-positive disease (approximately 2-4%), which indicates potential responsiveness to MET inhibitor therapy.5, 6, 7, 8, 9 Patients with these forms of lung cancer typically are female, are older in age, often have adenocarcinoma histology, and have poorer prognosis disease.4, 5, 6, 7, 9
Efficacy and safety of capmatinib in the treatment of metastatic NSCLC in patients whose tumors harbor a MET exon 14 skipping mutation were demonstrated in a nonrandomized, multiple-cohort, multinational, open-label phase 2 study (GEOMETRY mono-1) in adults with MET -dysregulated (i.e., MET exon 14 skipping mutation-positive or MET -amplified), wild-type epidermal growth factor receptor (EGFR), anaplastic lymphoma kinase ( ALK) -negative, locally advanced or metastatic (stage IIIB or stage IV) NSCLC with at least one measurable lesion.1, 3 The efficacy population for the indication of NSCLC with a MET exon 14 skipping mutation included 60 previously untreated patients and 100 patients who had received at least one prior therapy for NSCLC.1, 3 Patients received capmatinib 400 mg orally twice daily until disease progression or unacceptable toxicity occurred.1, 3 The primary measure of efficacy was overall response rate (complete plus partial responses) as assessed by a blinded independent review committee according to modified Response Evaluation Criteria in Solid Tumors (RECIST 1.1); the key secondary end point was duration of response.1, 3 The median age of patients in the efficacy population was 71 years (range: 48-90 years); 77% of patients were White, 61% were female, 99% had an ECOG performance status of 0 or 1, 61% had never smoked, 83% had adenocarcinoma histology, and 16% had brain metastases.1, 3 Among previously treated patients, 86% received one, 16% received two, and 3% received three prior lines of systemic chemotherapy.1 Most (86%) of the previously treated patients had received platinum-based chemotherapy.1 At the time of analysis, overall response rate in previously untreated or previously treated patients was 68 or 44%, respectively; complete response was achieved in 5 or 0% of patients, respectively.1, 3 The median duration of response in previously untreated or previously treated patients was 16.6 or 9.7 months, respectively;1, 3 the duration of response was 12 months or longer in 49 or 36% of patients, respectively.1
Dispensing and Administration Precautions
Capmatinib is administered orally twice daily without regard to meals.1 Capmatinib tablets should be swallowed whole and should not be broken, crushed, or chewed.1
If a dose of capmatinib is missed or vomited, patients should not double the dose or take extra doses.1 The next dose should be taken at the regularly scheduled time.1
Dosage of capmatinib hydrochloride is expressed in terms of capmatinib.1
The recommended adult dosage of capmatinib for the treatment of metastatic NSCLC that has a MET exon 14 skipping mutation is 400 mg twice daily.1 In the principal efficacy trial (GEOMETRY mono-1), capmatinib therapy was continued until disease progression or unacceptable toxicity occurred.1
Dosage Modification for Toxicity
If adverse reactions occur during capmatinib therapy, temporary interruption of therapy, dosage reduction, and/or discontinuance of the drug may be necessary.1 If dosage reduction is required, the dosage of capmatinib should be reduced as described in Table 1.1
Dose Reduction Level | Dosage Reduction after Recovery from Toxicity (Initial Dosage = 400 mg twice daily) |
|---|---|
First | Resume at 300 mg twice daily |
Second | Resume at 200 mg twice daily |
Third | Permanently discontinue drug |
If interstitial lung disease or pneumonitis occurs, capmatinib therapy should be permanently discontinued.1
If grade 3 elevations in ALT or AST concentrations occur in the absence of elevated total bilirubin concentrations, capmatinib therapy should be withheld until liver function test results return to baseline values.1 If recovery occurs within 7 days, capmatinib may be resumed at the same dosage.1 If recovery is delayed beyond 7 days, therapy may be resumed at the next lower dosage.1
If grade 4 elevations in ALT or AST concentrations occur in the absence of elevated total bilirubin concentrations, capmatinib therapy should be permanently discontinued.1
If elevations in ALT or AST concentrations exceeding 3 times the upper limit of normal (ULN) with total bilirubin concentrations exceeding 2 times the ULN occur in the absence of cholestasis or hemolysis, capmatinib therapy should be permanently discontinued.1
If grade 2 elevations in total bilirubin concentrations occur in the absence of elevated ALT and/or AST concentrations, capmatinib therapy should be withheld until total bilirubin concentrations return to baseline values.1 If recovery occurs within 7 days, capmatinib may be resumed at the same dosage.1 If recovery is delayed beyond 7 days, therapy may be resumed at the next lower dosage.1
If grade 3 elevations in total bilirubin concentrations occur in the absence of elevated ALT and/or AST concentrations, capmatinib therapy should be withheld until total bilirubin concentrations return to baseline values.1 If recovery occurs within 7 days, capmatinib may be resumed at the next lower dosage.1 Otherwise, capmatinib therapy should be permanently discontinued.1
If grade 4 elevations in total bilirubin concentrations occur in the absence of elevated ALT and/or AST concentrations, capmatinib therapy should be permanently discontinued.1
If grade 3 or 4 pancreatitis occur, capmatinib therapy should be permanently discontinued.1
If grade 4 elevations of lipase or amylase occur, permanently discontinue capmatinib therapy.1 If grade 3 elevations of lipase or amylase occur, withhold capmatinib until lipase and/or amylase elevations return to ≤ grade 2 or baseline.1 If recovered to baseline or ≤ grade 2 within 14 days, may resume capmatinib at a reduced dose; otherwise permanently discontinue.1
If any grade of hypersensitivity is suspected based on clinical judgment, withhold capmatinib therapy until resolution of the event.1 Permanently discontinue capmatinib in patients who develop serious hypersensitivity reactions.1
If any other grade 2 adverse reaction occurs, capmatinib therapy may be continued at the same dosa however, if the grade 2 adverse reaction is intolerable, interruption of capmatinib therapy may be considered.1 When the toxicity resolves, capmatinib may be resumed at the next lower dosage.1
If any other grade 3 adverse reaction occurs, capmatinib therapy should be interrupted.1 When the toxicity resolves, capmatinib may be resumed at the next lower dosage.1
If any other grade 4 adverse reaction occurs, capmatinib therapy should be permanently discontinued.1
No dosage adjustment is necessary in patients with mild to moderate renal impairment (creatinine clearance of 30-89 mL/minute).1 Insufficient data are available to provide dosage recommendations for patients with severe renal impairment (creatinine clearance less than 30 mL/minute).1 The manufacturer makes no specific dosage recommendations for geriatric patients or patients with hepatic impairment.1
The manufacturer states that there are no known contraindications to the use of capmatinib.1
Based on animal findings, capmatinib may increase the risk of photosensitivity reactions. 1 In the principal efficacy trial (GEOMETRY mono-1), patients receiving capmatinib were advised to use sunscreen and wear protective clothing to protect their skin from excessive exposure to sunlight.1
The manufacturer recommends that patients receiving capmatinib avoid unnecessary or excessive exposure to sunlight or artificial UV light (e.g., tanning beds, UVA/UVB treatment) and protect their skin from sun exposure (e.g., by wearing protective clothing or using sunscreen).1
Interstitial lung disease or pneumonitis, sometimes fatal, has been reported in patients receiving capmatinib.1 In the principal efficacy trial (GEOMETRY mono-1), interstitial lung disease or pneumonitis occurred in 4.8% of patients receiving capmatinib, was grade 3 in 1.9% of patients receiving the drug, and was fatal in one patient.1 Onset of manifestations of grade 3 or greater interstitial lung disease or pneumonitis occurred at a median of 1.8 months (range: approximately 6 days to 1.7 years) after initiating capmatinib therapy.1 Discontinuance of capmatinib therapy was necessary because of interstitial lung disease or pneumonitis in 2.4% of patients receiving the drug.1
Patients receiving capmatinib should be monitored for new or worsening symptoms indicative of interstitial lung disease or pneumonitis (e.g., dyspnea, cough, fever).1 Therapy with the drug should be withheld immediately in patients with suspected interstitial lung disease or pneumonitis and should be permanently discontinued if no other potential etiology is identified.1
Drug-induced hepatotoxicity has been reported in patients receiving capmatinib.1 In the principal efficacy trial (GEOMETRY mono-1), elevations in ALT or AST concentrations occurred in 15% of patients receiving capmatinib; grade 3 or 4 elevations in ALT or AST concentrations occurred in 7% of patients and permanent discontinuance of capmatinib was required because of elevations in ALT or AST concentrations in 0.8% of patients receiving the drug.1 The median time to onset of grade 3 or greater elevations in ALT or AST concentrations was 1.8 months (range: 0.5-46.4 months).1
The manufacturer states that liver function tests, including ALT, AST, and total bilirubin, should be monitored prior to initiating capmatinib therapy, every 2 weeks during the first 3 months of therapy, monthly thereafter, and as clinically indicated.1 More frequent testing is necessary in patients who develop aminotransferase or bilirubin elevations during therapy.1 If hepatotoxicity occurs, temporary interruption, dosage reduction, or discontinuance of capmatinib may be necessary.1
Elevations in amylase and lipase levels occurred in patients treated with capmatinib.1 In the principal efficacy trial (GEOMETRY mono-1), increased amylase/lipase occurred in 14% of patients treated with capmatinib; grade 3 and 4 increased amylase/lipase occurred in 7% and 1.9% of patients, respectively, and 3 patients (0.8%) discontinued the drug due to increased amylase/lipase.1 Grade 3 pancreatitis occurred in one patient (0.3%) and capmatinib was permanently discontinued for this event.1 The median time-to-onset of Grade 3 or higher increased amylase/lipase was 2 months (range: 0.03 to 31.1 months).1
The manufacturer recommends to monitor amylase and lipase at baseline and regularly during treatment with capmatinib.1 Based on the severity of the adverse reaction, it may be necessary to temporarily withhold, dose reduce, or permanently discontinue capmatinib.1
Serious hypersensitivity reactions occurred in patients treated with capmatinib in clinical trials other than GEOMETRY mono-1.1 Signs and symptoms of hypersensitivity included pyrexia, chills, pruritus, rash, decreased blood pressure, nausea, and vomiting.1 Based on the severity of the adverse reaction, it may be necessary to temporarily withhold or permanently discontinue capmatinib.1
Fetal/Neonatal Morbidity and Mortality
Capmatinib may cause fetal harm if administered to pregnant women based on its mechanism of action and animal findings.1 Although there are no available data regarding the risk of capmatinib use in pregnant women, animal reproduction studies have revealed evidence of embryofetal toxicity (i.e., decreased fetal body weight, incomplete ossification) and teratogenic effects (i.e., visceral and skeletal malformations) in rats and rabbits at exposure levels of approximately 0.016-0.6 times the human exposure at the recommended dosage.1
Pregnancy should be avoided during capmatinib therapy.1 The manufacturer states that a pregnancy test should be performed prior to initiation of capmatinib in women of reproductive potential and that such women should use effective contraceptive methods while receiving the drug and for 1 week after the last dose.1 In addition, men who are partners of such women should use effective contraceptive methods during therapy and for 1 week after the last dose.1 If capmatinib is used during pregnancy or if the patient or their partner becomes pregnant during therapy, the patient should be apprised of the potential fetal hazard.1
Capmatinib may cause fetal harm if administered to pregnant women based on its mechanism of action and animal findings.1
It is not known whether capmatinib or its metabolites are distributed into human milk.1 The effects of the drug on breast-fed infants or on milk production also are unknown.1
Because of the potential for serious adverse reactions to capmatinib in breast-fed infants, women should be advised not to breast-feed while receiving the drug and for 1 week after the last dose.1
Safety and efficacy of capmatinib have not been established in pediatric patients.1
In the principal efficacy trial (GEOMETRY mono-1), 61% of patients with metastatic non-small cell lung cancer (NSCLC) who received capmatinib were 65 years of age or older and 18% were 75 years of age or older.1 No overall differences in safety and efficacy were observed between these geriatric patients and younger adults.1
In a population pharmacokinetic analysis, age (range of 26-90 years) did not have a substantial effect on the pharmacokinetics of capmatinib.1
Population pharmacokinetic analysis suggests that the pharmacokinetics of capmatinib are not substantially altered in patients with mild, moderate, or severe hepatic impairment (Child-Pugh class A, B, or C).1
Population pharmacokinetic analysis suggests that the pharmacokinetics of capmatinib are not substantially altered in patients with mild to moderate renal impairment (creatinine clearance of 30-89 mL/minute).1 The effect of severe renal impairment (creatinine clearance less than 30 mL/minute) on the pharmacokinetics of capmatinib has not been established.1
The most common adverse reactions (≥20% incidence) include edema, nausea, musculoskeletal pain, fatigue, vomiting, dyspnea, cough, and decreased appetite.1
Capmatinib is metabolized principally by cytochrome P-450 (CYP) isoenzyme 3A4 and aldehyde oxidase.1
In vitro, capmatinib reversibly inhibits multidrug and toxin extrusion protein (MATE) 1 and 2K, but does not inhibit organic anion transport protein (OATP) 1B1 or 1B3, organic cation transporter (OCT) 1, organic anion transporter (OAT) 1 or 3, or multidrug resistance-associated protein 2 (MRP2).1 In vitro, capmatinib is a substrate of P-glycoprotein (P-gp), but is not a substrate of breast cancer resistance protein (BCRP) or MRP2.1
Drugs Affecting Hepatic Microsomal Enzymes
Concomitant use of capmatinib with potent inhibitors of CYP3A may result in increased systemic exposure to capmatinib and increased adverse effects.1 When the potent CYP3A inhibitor itraconazole (200 mg daily) was administered concomitantly with capmatinib (single 200-mg dose), area under the concentration-time curve (AUC) of capmatinib was increased by 42% but peak plasma concentrations were not affected.1, 9
The manufacturer states that patients receiving current therapy with capmatinib and a potent CYP3A4 inhibitor (e.g., itraconazole) should be monitored closely for adverse effects of capmatinib.1
Concomitant use of capmatinib with moderate or potent inducers of CYP3A may result in decreased plasma concentrations of capmatinib and reduced capmatinib efficacy.1 When the potent CYP3A inducer rifampin (600 mg daily) was administered concomitantly with capmatinib (single 400-mg dose), AUC and peak plasma concentration of capmatinib were decreased by 67 and 56%, respectively.1, 9 Concomitant administration of capmatinib with the moderate CYP3A inducer efavirenz is expected to decrease the AUC and peak plasma concentration of capmatinib by 44 and 34%, respectively.1
Concomitant use of capmatinib with moderate or potent CYP3A inducers should be avoided.1
Drugs Metabolized by Hepatic Microsomal Enzymes
Concomitant use of capmatinib and substrates of CYP1A2 may result in increased plasma concentrations of the CYP1A2 substrate and possible adverse effects.1 When the CYP1A2 substrate caffeine (single 100-mg dose) was administered concomitantly with capmatinib (400 mg twice daily), AUC of caffeine was increased by 134%; peak plasma concentrations of caffeine were not affected.1, 9
Concomitant use of capmatinib with CYP1A2 substrates that have a narrow therapeutic index should be avoided.1 If such concomitant use cannot be avoided, the manufacturer recommends reducing the dosage of the substrate drug.1
Concomitant administration of capmatinib and the CYP3A substrate midazolam did not result in clinically important changes in exposure to midazolam.1
Substrates of Drug Transport Systems
Concomitant use of capmatinib and substrates of P-gp may result in increased plasma concentrations of the P-gp substrate and possible adverse effects.1 When the P-gp substrate digoxin was administered concomitantly with capmatinib (400 mg twice daily), AUC and peak plasma concentration of digoxin were increased by 47 and 74%, respectively.1, 9
Concomitant use of capmatinib with P-gp substrates that have a narrow therapeutic index should be avoided.1 If such concomitant use cannot be avoided, the manufacturer recommends reducing the dosage of the P-gp substrate drug.1
Concomitant use of capmatinib and substrates of BCRP may result in increased plasma concentrations of the BCRP substrate and possible adverse effects.1 When the BCRP substrate rosuvastatin was administered concomitantly with capmatinib (400 mg twice daily), AUC and peak plasma concentration of rosuvastatin were increased by 108 and 204%, respectively.1, 9
Concomitant use of capmatinib with BCRP substrates that have a narrow therapeutic index should be avoided.1 If such concomitant use cannot be avoided, the manufacturer recommends reducing the dosage of the BCRP substrate drug.1
Concomitant use of capmatinib and substrates of MATE1 or MATE2K may result in increased plasma concentrations of the MATE1 or MATE2K substrate and possible adverse effects.1
Concomitant use of capmatinib with MATE1 or MATE2K substrates that have a narrow therapeutic index should be avoided.1 If such concomitant use cannot be avoided, the manufacturer recommends reducing the dosage of the MATE1 or MATE2K substrate drug.1
Drugs Affecting Gastric Acidity
Concomitant administration of capmatinib (single 600-mg dose) and the proton-pump inhibitor rabeprazole (20 mg daily) decreased the AUC and peak plasma concentration of capmatinib by 25 and 38%, respectively.1, 9
Capmatinib, a potent and selective inhibitor of mesenchymal-epithelial transition (MET) receptor tyrosine kinase, is an antineoplastic agent.1, 3, 4, 5, 9 Activation of MET tyrosine kinase, occurring through overexpression, MET amplification, or the exon 14 skipping mutation, is thought to initiate a cascade of intracellular signaling events leading to cell proliferation and influencing processes critical to cell survival and tumor progression (e.g., angiogenesis, apoptosis, metastasis).1, 4, 5, 8, 9 MET exon 14 skipping mutations are present in approximately 2-4% of patients with non-small cell lung cancer (NSCLC).5, 6, 7, 8, 9 Capmatinib inhibits MET phosphorylation caused by the binding of hepatocyte growth factor or by MET amplification, resulting in downregulation of downstream MET signaling proteins and inhibition of proliferation and survival of MET-dependent tumor cells.1, 6, 9
Following oral administration, peak plasma concentrations of capmatinib are achieved in approximately 1-2 hours.1 The estimated extent of absorption of a single 400-mg oral dose is more than 70%.1 The area under the plasma concentration-time curve (AUC) and peak plasma concentration of capmatinib increase in a dose-proportional manner over a dosage range of 200-400 mg twice daily.1 Steady-state concentrations of capmatinib are reached within 3 days of twice-daily dosing, with a mean accumulation ratio of 1.5.1 In healthy individuals, administration of capmatinib with a high-fat meal increased the AUC of capmatinib by 46% compared with administration in the fasted state, but did not alter the peak plasma concentration of the drug;1 administration with a low-fat meal did not substantially alter exposure.1 In cancer patients receiving capmatinib 400 mg twice daily, exposure was similar following administration in the fed or fasted state.1 Capmatinib is metabolized mainly by cytochrome P-450 (CYP) isoenzyme 3A4 and aldehyde oxidase.1 Capmatinib crosses the blood-brain barrier.3, 6 Capmatinib is 96% bound to plasma proteins, and binding is independent of capmatinib concentration.1 Following oral administration of a single radiolabeled dose of capmatinib, approximately 78% of the radioactivity was recovered in feces and 22% was recovered in urine; unchanged drug accounted for 42% of the dose recovered in feces and a negligible amount of the dose recovered in urine.1 The effective elimination half-life of capmatinib is 6.5 hours.1 The pharmacokinetics of capmatinib are not affected by age, sex, race, or body weight.1
Importance of advising patients to take capmatinib exactly as prescribed and of not altering the dosage or discontinuing the therapy unless advised to do so by their clinician.1
Importance of advising patients to swallow capmatinib tablets whole and not to chew, crush, or split the tablets.1 If a dose is missed or if vomiting occurs after a dose is administered, the next dose should be taken at the regularly scheduled time; the missed dose should not be taken, and an additional dose should not be administered to replace the vomited dose.1
Risk of interstitial lung disease or pneumonitis.1 Importance of immediately informing clinician if new or worsening respiratory symptoms (e.g., dyspnea, cough) or fever occurs.1
Risk of hepatotoxicity; importance of liver function test monitoring.1 Importance of advising patients to immediately report possible symptoms of hepatotoxicity (e.g., jaundice, dark or “tea-colored” urine, right upper quadrant pain, light-colored stool, decreased appetite, nausea, vomiting, weakness, fatigue, confusion) to their clinician.1
Risk of pancreatic toxicity; inform patients of the need for lab testing to monitor pancreatic function.1 Advise patients to immediately inform their clinician if signs and symptoms of pancreatitis occur.1
Risk of hypersensitivity reactions. Advise patients to stop taking capmatinib and immediately contact their clinician if signs and symptoms (e.g., pyrexia, chills, pruritus, rash, decreased blood pressure, nausea and vomiting) of hypersensitivity occur.1
Possibility of photosensitivity reactions; importance of using protective measures (e.g., wearing protective clothing, using sunscreen) and limiting direct exposure to UV light during capmatinib therapy.1
Risk of fetal harm.1 Necessity of advising women of reproductive potential and men who are partners with such women that they should use effective contraceptive methods while receiving the drug and for 1 week after the last dose.1 Importance of patients informing their clinicians if they or their partners are pregnant or think they may be pregnant.1 If pregnancy occurs, advise patient of potential risk to fetus.1
Importance of advising women to avoid breast-feeding while receiving capmatinib therapy and for 1 week after the last dose.1
Importance of informing clinicians of existing or contemplated concomitant therapy, including prescription and OTC drugs and herbal supplements, as well as any concomitant illnesses.1
Importance of informing patients of other important precautionary information.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.
Routes | Dosage Forms | Strengths | Brand Names | Manufacturer |
|---|---|---|---|---|
Oral | Tablets, film-coated | 150 mg (of capmatinib) | Tabrecta® | Novartis |
200 mg (of capmatinib) | Tabrecta® | Novartis |
AHFS® Drug Information. © Copyright, 1959-2026, Selected Revisions August 25, 2023. American Society of Health-System Pharmacists, Inc., 4500 East-West Highway, Suite 900, Bethesda, MD 20814.
1. Novartis Pharmaceuticals Corporation. Tabrecta® (capmatinib hydrochloride) tablets prescribing information. East Hanover, NJ: 2023 Mar.
2. Food and Drug Administration. Search orphan drug designations and approvals. From FDA website. Accessed 2021 Feb 5. [Web]
3. Wolf J, Seto T, Han JY et al. Capmatinib in MET Exon 14-Mutated or MET-Amplified Non-Small-Cell Lung Cancer. N Engl J Med . 2020; 383:944-57. [PubMed 32877583]
4. Bang YJ, Su WC, Schuler M et al. Phase 1 study of capmatinib in MET-positive solid tumor patients: Dose escalation and expansion of selected cohorts. Cancer Sci . 2020; 111:536-47. [PubMed 31778267]
5. Schuler M, Berardi R, Lim WT et al. Molecular correlates of response to capmatinib in advanced non-small-cell lung cancer: clinical and biomarker results from a phase I trial. Ann Oncol . 2020; 31:789-97. [PubMed 32240796]
6. Vansteenkiste JF, Van De Kerkhove C, Wauters E et al. Capmatinib for the treatment of non-small cell lung cancer. Expert Rev Anticancer Ther . 2019; 19:659-71. [PubMed 31368815]
7. Awad MM, Oxnard GR, Jackman DM et al. MET Exon 14 Mutations in Non-Small-Cell Lung Cancer Are Associated With Advanced Age and Stage-Dependent MET Genomic Amplification and c-Met Overexpression. J Clin Oncol . 2016; 34:721-30. [PubMed 26729443]
8. Bylicki O, Paleiron N, Assié JP et al. Targeting the MET-Signaling Pathway in Non-Small-Cell Lung Cancer: Evidence to Date. Onco Targets Ther . 2020; 13:5691-5706. [PubMed 32606781]
9. US Food and Drug Administration. Center for Drug Evaluation and Research. Application number 213591Orig1s000: Multi-discipline review. From FDA website. [Web]
10. Institute for Safe Medication Practices. ISMP list of high-alert medications in acute care settings. [Web]. Accessed 2023 Aug 23.