TP Therapeutics pipeline includes potent inhibitors targeting established oncogene drivers, and resistance issues to treatments including secondary resistant mutations, bypass mechanisms, and EMT. We also work on newly identified disease-driven targets, and targets regulating tumor microenvironment and tumor immunity.
Our leading project TPX-0005 is now in clinical development (TRIDENT-1, NCT03093116). More information about TRIDENT-1 is available at ClinicalTrials.gov. Here is the official title for this clinical trial:
A Phase 1/2, Open-Label, Multi-Center, First-in-Human Study of the Safety, Tolerability, Pharmacokinetics, and Anti-Tumor Activity of TPX-0005 in Patients with Advanced Solid Tumors Harboring ALK, ROS1, or NTRK1-3 Rearrangements (TRIDENT-1)
Here are three TPX-0005 posters on NTRK, ROS1, and ALK presented at AACR-NCI-EORTC International Conference on Molecular Targets and Cancer Therapeutics: Discovery, Biology, and Clinical Applications, October 26-30, 2017, Philadelphia, Pennsylvania
- TPX-0005, a highly potent TRK inhibitor, effectively overcomes clinical-resistance TRK mutations including solvent front mutants TRKA G595R, TRKB G639R, and TRKC G623R
- TPX-0005, a supreme ROS1 inhibitor, overcomes crizotinib-resistant ROS1 mutations including solvent front mutation G2032R and gatekeeper mutation L2026M
- TPX-0005, a polypharmacology inhibitor, overcomes ALK treatment resistances from acquired mutations, bypass signaling and EMT
Here is a recent poster on TPX-0005 at The IASLC 18th World Conference on Lung Cancer (WCLC), October 15-18, 2017, Yokohama, Japan.
- TPX-0005 with an EGFR tyrosine kinase inhibitor (TKI) overcomes innate resistance in EGFR mutant NSCLC
Here are two AACR abstracts on TPX-0005:
- Ending the endless acquired tyrosine kinase resistance mutations — Design of TPX-0005, a multi-target ALK/ROS1/TRK inhibitor with broad spectrum activity against wild-type and mutants including ALK G1202R, ROS1 G2032R and TRKA G595R
- The novel, rationally-designed, ALK/SRC inhibitor TPX-0005 overcomes multiple acquired resistance mechanisms to current ALK inhibitors
For more detailed information, please contact us at email@example.com.