BI-3406 | SOS1 inhibitor
Available Options
| Size: | Price | Quantity | |
|---|---|---|---|
| 5 mg | $60.00 | ||
| 25 mg | $225.00 |
BI-3406 (2230836-55-0) is a potent (IC50 = 5 nM), selective, and orally bioavailable SOS1 inhibitor.1 It blocks SOS1 interaction with KRAS preventing activation of KRAS. BI-3406 was active against multiple cancer cell types and xenograft models harboring various KRAS mutant alleles including G12C,V,S,A,and G13D. It displayed strong synergistic effects with the MEK inhibitor trametinib1,2 and this combination was able to overcome resistance to the KRAS inhibitors sotorasib and adagrasib3. BI-3406 acted synergistically with the KRAS inhibitor adagrasib in KRAS G12C mutant lung and colorectal cancer models.4
References/Citations:
- Hofmann et al. (2020), BI-3406, a potent and selective SOS1::KRAS interaction inhibitor, is effective in KRAS-driven cancers through combined MEK inhibition; Cancer Discov. 11 142
- Ma et al. (2022), Inhibition of KRAS, MEK and PI3K Demonstrate Synergistic Anti-Tumor Effects in Pancreatic Ductal Adenocarcinoma Cell Lines; Cancers (Basel) 14 4467
- Koga et al. (2021), KRAS Secondary Mutations That Confer Acquired Resistance to KRAS G12C Inhibitors, Sotorasib and adagrasib, and Overcoming Strategies: Insights From In Vitro Experiments; J. Thorac. Oncol. 16 1321
- Thatikonda et al. (2024), Co-targeting SOS1 enhances the antitumor effects of KRASG12C inhibitors by addressing intrinsic and acquired resistance; Nat. Cancer 5 1352
C23H25F3N4O3
>98% HPLC
NMR: (Conforms)
Safety Data Sheet:
Product Data Sheet:
Materials provided by Focus Biomolecules are for laboratory research use only and are not intended for human or veterinary applications. Please note that we do not sell to individuals and that all orders placed by non-research organizations will incur a $20 restocking/refund fee
BI-3406 (2230836-55-0) is a potent (IC50 = 5 nM), selective, and orally bioavailable SOS1 inhibitor.1 It blocks SOS1 interaction with KRAS preventing activation of KRAS. BI-3406 was active against multiple cancer cell types and xenograft models harboring various KRAS mutant alleles including G12C,V,S,A,and G13D. It displayed strong synergistic effects with the MEK inhibitor trametinib1,2 and this combination was able to overcome resistance to the KRAS inhibitors sotorasib and adagrasib3. BI-3406 acted synergistically with the KRAS inhibitor adagrasib in KRAS G12C mutant lung and colorectal cancer models.4
References/Citations:
- Hofmann et al. (2020), BI-3406, a potent and selective SOS1::KRAS interaction inhibitor, is effective in KRAS-driven cancers through combined MEK inhibition; Cancer Discov. 11 142
- Ma et al. (2022), Inhibition of KRAS, MEK and PI3K Demonstrate Synergistic Anti-Tumor Effects in Pancreatic Ductal Adenocarcinoma Cell Lines; Cancers (Basel) 14 4467
- Koga et al. (2021), KRAS Secondary Mutations That Confer Acquired Resistance to KRAS G12C Inhibitors, Sotorasib and adagrasib, and Overcoming Strategies: Insights From In Vitro Experiments; J. Thorac. Oncol. 16 1321
- Thatikonda et al. (2024), Co-targeting SOS1 enhances the antitumor effects of KRASG12C inhibitors by addressing intrinsic and acquired resistance; Nat. Cancer 5 1352
Calculate the molar concentration, mass or volume in a solution.
Concentration × Volume × Molecular Weight = Mass
