Vitrakvi (larotrectinib sulfate)

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Last reviewed · Source: First Databank (FDB) drug data

Overview

Larotrectinib, a potent and selective inhibitor of tropomyosin receptor kinase (TRK) A, TRK-B, and TRK-C, is an antineoplastic agent.

Larotrectinib, a potent and selective inhibitor of tropomyosin receptor kinase (TRK) A, TRK-B, and TRK-C, is an antineoplastic agent. The TRK family of tyrosine kinases (encoded by the neurotrophic receptor tyrosine kinase genes NTRK1, NTRK2, and NTRK3) are involved in the initiation of various cascades of intracellular signaling events (i.e., Ras/MAPK/ERK, PI3K/Akt, and PLCgamma1/Pkc signal transduction pathways), which leads to cell proliferation, differentiation, apoptosis, and regulation of processes critical to neuron survival in the central and peripheral nervous systems. Chromosomal rearrangements of the NTRK1, NTRK2, and NTRK3 genes result in fusions with an unrelated gene.

These NTRK gene fusions encode a constitutively active chimeric TRK oncogenic fusion protein resulting in dysregulation of TRK signaling and subsequent tumorigenesis. In vitro biochemical assays have shown that larotrectinib inhibits the activity of wild-type TRK-A, TRK-B, and TRK-C. In vitro and in vivo, larotrectinib has demonstrated antitumor activity in cell lines with TRK expression from constitutive activation, deletion of a protein regulatory domain, or overexpression of wild-type TRK.

Larotrectinib also has demonstrated inhibition of tyrosine kinase nonreceptor 2 (TNK2).

Clinical resistance to larotrectinib has been attributed to secondary point mutations of the NTRK kinase domain in 90% of cases. Larotrectinib has shown minimal activity in cell lines with point mutations in the TRK-A kinase domain, including the acquired resistance mutation G595R. Acquired resistance to larotrectinib also has been identified in cell lines with G623R, G696A, or F617L point mutations in the TRK-C kinase domain.

Following oral administration of larotrectinib capsules, systemic exposure to larotrectinib increases in a dose-proportional manner over a dose range of 100-400 mg and increases in a slightly more than dose-proportional manner over a dose range of 600-900 mg. Following oral administration of larotrectinib capsules at a dosage of 100 mg twice daily, peak plasma concentrations of the drug were achieved in approximately 1 hour and steady-state concentrations were achieved within 3 days. The mean absolute oral bioavailability of larotrectinib capsules was 34%.

The area under the plasma-concentration time curve (AUC) for larotrectinib oral solution was similar to the AUC for larotrectinib capsules; peak plasma concentrations were 36% higher for larotrectinib oral solution compared with larotrectinib capsules. Administration of larotrectinib capsules (single 100-mg dose) with a high-fat meal decreased peak plasma concentrations by 35% and delayed the time to peak plasma concentrations by 2 hours compared with administration in the fasted state, but did not substantially affect the extent of absorption. Larotrectinib is metabolized principally by cytochrome P-450 (CYP) isoenzyme 3A4.

Larotrectinib is 70% bound to plasma proteins, and binding is independent of larotrectinib concentration. Following oral administration of a single 100-mg radiolabeled dose of larotrectinib, 58% of the dose was recovered in feces (5% as unchanged drug) and 39% was recovered in urine (20% as unchanged drug). The terminal half-life of larotrectinib is 2.9 hours.

The pharmacokinetics of larotrectinib do not appear to be affected by age (range of 28 days to 82 years), sex, or body weight (range of 3.8-179 kg).

USES: Larotrectinib is used to treat cancer. It works by slowing or stopping the growth of cancer cells.

Generic name: larotrectinib sulfate
Pronunciation: (LAR-oh-TREK-ti-nib)

Reference product & biosimilars

No reference, biosimilar or interchangeable associated with this drug.

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Indications

The following indications are listed for Vitrakvi:

  • Solid Tumor With Neurotrophic Receptor Tyrosine Kinase (NTRK) Gene Fusion

Also known as: Solid Tumor With Neurotrophic Receptor Tyrosine Kinase Gene Fusion.

Dosing

Dosage of larotrectinib sulfate is expressed in terms of larotrectinib.

If a grade 2 or higher liver function test abnormalities occur, refer to Table 2. For all other grade 3 or 4 adverse reactions, larotrectinib therapy should be withheld. If the grade 3 or 4 adverse reaction resolves to grade 1 or baseline within 4 weeks of withholding larotrectinib, the drug should be resumed at a reduced dosage (or discontinued) as described in Table 1. If the grade 3 or 4 adverse reaction does not resolve within 4 weeks of withholding larotrectinib, the drug should be permanently discontinued.

Table 1. Recommended Dosage Reductions for Larotrectinib Toxicity.

Dosage Modification Dosage Modification Dosage Modification after Recovery from after Recovery from Toxicity Adult and Toxicity Pediatric Pediatric Patients with Patients with BSA <1 m2 BSA >=1 m2 (Starting (Starting Dosage = 100 Dosage = 100 mg twice mg/m2 twice daily) daily) First Restart at 75 mg twice Restart at 75 mg/m2 daily twice daily Second Restart at 50 mg twice Restart at 50 mg/m2 daily twice daily Third Restart at 100 mg once Restart at 25 mg/m2 daily twice daily Fourth Permanently discontinue Permanently discontinue larotrectinib larotrectinib

If BSA increases to >1 m2 in pediatric patients following dosage reduction to 25 mg/m2twice daily, do not increase dosage. Maximum dose should be 25 mg/m2twice daily at the third dosage modification

Table 2. Dosage Modifications for Hepatotoxicity

Severity Dosage Modification AST or ALT >=5 times ULN with Withhold until recovery to grade 1 bilirubin <=2 times ULN or baseline then resume therapy at the next lower dose level Permanently discontinue if grade 4 AST and/or ALT elevation occurs after resuming therapy AST or ALT >3 times ULN with total Permanently discontinue therapy bilirubin >2 times ULN in the absence of alternative etiologies

Drug interactions

Larotrectinib is metabolized principally by cytochrome P-450 (CYP) isoenzyme 3A4.

In vitro studies indicate that larotrectinib is an inhibitor of CYP3A4. In vitro, larotrectinib does not inhibit or induce CYP isoenzymes 1A2, 2B6, 2C8, 2C9, 2C19, or 2D6 at clinically relevant concentrations.

In vitro, larotrectinib is a substrate of the efflux transporters P-glycoprotein (P-gp) and breast cancer resistance protein (BCRP), but is not a substrate for organic anion transporter (OAT) 1, OAT3, organic cation transporter (OCT) 1, OCT2, organic anion transport protein (OATP) 1B1, or OATP1B3. In vitro studies indicate that larotrectinib does not inhibit P-gp, BCRP, OAT1, OAT3, OCT1, OCT2, OATP1B1, OATP1B3, bile salt export pump (BSEP), multidrug and toxin extrusion (MATE) transporter 1, and MATE2K at clinically relevant concentrations.

Contraindications

*None.

Adverse reactions

Adverse effects reported in >20% of patients receiving larotrectinib include increased AST concentrations, increased ALT concentrations, anemia, hypoalbuminemia, musculoskeletal pain, increased alkaline phosphatase concentrations, leukopenia, lymphopenia, neutropenia, hypocalcemia, fatigue, vomiting, cough, constipation, pyrexia, diarrhea, nausea, abdominal pain, dizziness, and rash.

Precautions

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ICD codes

No ICD codes are available for this drug.

Formulary status

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Last reviewed · Source: First Databank (FDB) drug data