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Ras is the name given to a family of related proteins which is ubiquitously expressed in all cell lineages and organs. All Ras protein family members belong to a class of protein called small GTPase, and are involved in transmitting signals within cells. Ras is the prototypical member of the Ras superfamily of proteins, which are all related in 3D structure and regulate diverse cell behaviours. When Ras is 'switched on' by incoming signals, it subsequently switches on other proteins, which ultimately turn on genes involved in cell growth, differentiation and survival. As a result, mutations in ras genes can lead to the production of permanently activated Ras proteins. This can cause unintended and overactive signalling inside the cell, even in the absence of incoming signals. Because these signals result in cell growth and division, overactive Ras signaling can ultimately lead to cancer. The 3 Ras genes in humans (HRAS,KRAS, and NRAS) are the most common oncogenes in human cancer; Ras inhibitors are being studied as a treatment for cancer, and other diseases with Ras overexpression.

Cat. No. Product Name CAS No. Information



BI-2852 is a KRAS inhibitor for the switch I/II pocket (SI/II-pocket) by structure-based drug design with nanomolar affinity. BI-2852 is mechanistically distinct from covalent KRASG12C inhibitor (binds to switch II pocket) because it binds to a different pocket present in both the active and inactive forms of KRAS. BI-2852 blocks GEF, GAP, and effector interactions with KRAS, leading to inhibition of downstream signaling and an antiproliferative effect in KRAS mutant cells.




pan-Ras inhibitor 3144 (Compound 3144) is a multivalent small-molecule, pan-RAS inhibitor with Kd of 4.7/17/6.6/3.7 uM for KRAS G12D/KRAS wt/HRAS/NRAS respectively; shows weak bindinf for RRAS2 (Kd=24 uM) and no activity for other small GTPases in the RAS superfamily; exhibits lethality in cells partially dependent on expression of RAS proteins; has suitable ADME properties and displays anti-tumor activity in xenograft mouse of pancreatic cancer; orally bioavailable.




ARS-1630 is the R-conformational atropisomer of ARS-1620, 1,000-fold less potent than ARS-1620 (1.2 ± 0.6 M-1s-1) and thus acts as a unique inactive control compound.




ARS-1620 is a potent, specific and covalent KRAS G12C inhibitor with an observed rate of 1,100±200 M-1S-1, shows >10-fold improved potency over the initial ARS-853; inhibits RAS signaling with IC50 of 120 nM, exhibits a half maximal G12C target engagement (TE50) at 0.3 uM and near complete engagement at 3.0 uM across a panel of cell lines harboring the mutant allele; achieves rapid and sustained in vivo target occupancy to induce tumor regression, and is a novel generation of KRASG12C-specific inhibitor with promising therapeutic potential.




ARS1323 is a racemic mixture of ARS-1620/R-atropisomer, ARS-1620 is a potent, specific and covalent KRAS G12C inhibitor with >10-fold improved potency over the initial ARS-853.


K-Ras G12C-IN-3


A novel and irreversible inhibitor of mutant K-ras G12C.




ARS-853 is a mutant-specific, covalent inhibitor of KRAS(G12C); engages KRASG12C in biochemical assay with a rate constant of 76 M-1s-1, > 600-fold improvement compared with Compound 12 (Ostrem JM, Nature 2013;503:548–51.); inhibits growth of H358 cells; the first direct KRAS inhibitor shown to selectively inhibit KRAS in cells with potency in the range of a drug candidate.


K-Ras G12C-IN-2


A novel and irreversible inhibitor of mutant K-ras G12C.


K-Ras G12C-IN-1


A novel and irreversible inhibitor of mutant K-ras G12C.




6H05 is a selective, allosteric inhibitor of oncogenic mutant K-Ras(G12C), an intermediate for the synthesis of other oncogenic K-Ras(G12C) inhibitors.

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