What is the mechanism of action of larotrectinib?

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Mechanism of Action of Larotrectinib

Larotrectinib is an ATP-competitive, small-molecule inhibitor that selectively and potently targets the tropomyosin receptor kinases TRKA, TRKB, and TRKC, with IC50 values in the range of 5-11 nM. 1

Molecular Target and Selectivity

  • Larotrectinib inhibits all three TRK proteins (TRKA, B, and C) encoded by the NTRK1, NTRK2, and NTRK3 genes with half-maximal inhibitory concentrations between 5-11 nM 1

  • The drug demonstrates exceptional selectivity, with binding affinities over 100-fold greater for TRK proteins compared to a panel of other kinases 2

  • In comprehensive enzyme assays, larotrectinib inhibited no other tested kinases at concentrations up to 500-1,000 nM, with only one other kinase (TNK2) inhibited at approximately 100-fold higher concentration 2, 1

Mechanism of Oncogenic Inhibition

  • Larotrectinib works by blocking constitutively-activated chimeric TRK fusion proteins that result from chromosomal rearrangements involving in-frame fusions of NTRK genes with various partner genes 1

  • These NTRK gene fusions produce fusion proteins with constitutive tyrosine kinase activity that act as primary oncogenic drivers, promoting cell proliferation and survival in tumor cells 2

  • The drug demonstrated anti-tumor activity specifically in cells with constitutive TRK activation resulting from gene fusions, deletion of protein regulatory domains, or TRK protein overexpression 1

Clinical Implications of the Mechanism

  • Larotrectinib's ATP-competitive mechanism allows it to bind to the ATP-binding pocket of the TRK kinase domain, preventing downstream oncogenic signaling 2

  • The drug had minimal activity against cells with point mutations in the TRKA kinase domain, including the clinically identified acquired resistance mutation G595R 1

  • Known resistance mutations in the TRKC kinase domain include G623R, G696A, and F617L, which can develop after initial response to treatment 1

  • The high selectivity translates to a favorable safety profile, as the drug does not significantly inhibit off-target kinases that could cause additional toxicities 2

References

Guideline

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Dr.Oracle Medical Advisory Board & Editors, 2025

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This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

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