g12v

Rineterkib (ERK-IN-1) is an inhibitor of RAF and ERK1/2 activating mutations in the MAPK pathway.

BI-2493 is a highly selective pan-KRAS inhibitor and structural analog of BI-2865.BI-2493 exhibits antitumor activity and inhibits tumor cell growth and can be used in the study of cancerous diseases.BI-2493 is a highly selective pan-KRAS inhibitor and structural analog of BI-2865.

Daraxonrasib (RMC-6236) is an orally effective and novel triple complex RAS (ON) MULTI inhibitor, which is a potent non covalent inhibitor of multiple RAS variants in GTP binding state. RMC-6236 has anti-tumor activity and can be used in research related to RAS driven tumors. With rich experience in compound synthesis, we can provide fast customized synthesis services for this product according to your research needs.

BI-2865 is a non-covalent pan-KRAS inhibitor.BI-2865 binds to KRAS WT, G12C, G12D, G12V, and G13D mutants with KD values of 6.9, 4.5, 32, 26, and 4.3 nM, respectively.BI-2865 showed antiproliferative activity in BaF3 cells expressing KRAS G12C, G12D, or G12V mutants[1] . BI-2865 showed antiproliferative activity on BaF3 cells expressing KRAS G12C, G12D or G12V mutants, with an average IC50 value of approximately 140 nM.[1]

AMG410 is a non-covalent, dual-modality KRAS inhibitor effective against both GDP (OFF) and GTP (ON) binding, with Kd (GDP) of 1 nM and Kd (GTP) of 22 nM, capable of blocking KRAS independently of the cell cycle. AMG410 does not affect HRAS and NRAS2, and exhibits high potency against KRAS G12D, G12V, G12C, G13D, and other mutants, with an IC₅₀ of 1–4 nM. It induces tumour regression and reduces phosphorylated ERK levels in KRAS-mutant cancer models.

KRAS inhibitor-31 (compound 33), a potent agent targeting KRAS, exhibits K D (SPR) values of 0.019 nM for KRas G12D, 0.019 nM for KRas G12C, and 0.096 nM for KRas G12V, illustrating its efficacy across these variants.

KRAS inhibitor-37 (compound 2) is a potent inhibitor of KRAS, exhibiting low dissociation constants (KD) with various KRAS mutations: wild type (0.004 nM), G12D (0.041 nM), G12C (0.019 nM), and G12V (0.144 nM). This compound effectively inhibits cell proliferation, demonstrating half-maximal inhibitory concentrations (IC50) ranging from <2 nM to 14 nM in H358, SW620, and PANC08.13 cell lines. KRAS inhibitor-37 holds potential for cancer research applications.

PROTAC K-Ras degrader-2 (compound 48) is a broad-spectrum KRAS mutant PROTAC degrader that demonstrates an IC50 of ≤200 nM for KRAS G12V/RAF1. Additionally, PROTAC K-Ras degrader-2 achieves a DC50 of ≤200 nM in degrading SW620 KRAS G12D and inhibits the growth of SW620 3D cells with an IC50 of ≤20 nM.

pan-KRAS-IN-13 (compound 2) is a potent inhibitor of KRAS, exhibiting IC50 values of 2.75 nM and 2.89 nM for its G12D and G12V mutations, respectively.

KRAS-IN-43 (Compound 9) is a broad-spectrum KRAS inhibitor with IC50 values of 0.15 μM for KRASG12V, 0.14 μM for KRASG12C, and 0.47 μM for wild-type KRAS. It disrupts the interaction between KRAS and cRAF and suppresses ERK phosphorylation. KRAS-IN-43 shows potential for research in KRAS mutation-associated cancers, including pancreatic, colorectal, and lung cancers.

SOS1-IN-7 (compound 18-p1) is a potent SOS1 inhibitor with IC50 values of 20 nM for SOS1-G12D and 67 nM for SOS1-G12V.

SOS1-IN-6 (compound 33-P1) is a potent inhibitor of SOS1, exhibiting an IC50 of 14.9 nM on SOS1-G12D and 73.3 nM on SOS1-G12V.

SOS1-IN-8 is an inhibitor of SOS1 and acts on SOS1-G12D (IC50: 11.6 nM) and SOS1-G12V (IC50: 40.7 nM).

SAH-SOS1A TFA is a peptide-based SOS1/KRAS protein interaction inhibitor. SAH-SOS1A TFA binds to wild-type and mutant KRAS (G12D, G12V, G12C, G12S, and Q61H) with nanomolar affinity ( EC 50 =106-175 nM). SAH-SOS1A TFA directly and independently blocks nucleotide association. SAH-SOS1A TFA impairs KRAS-driven cancer cell viability and exerts its effects by on-mechanism blockade of the ERK-MAPK phosphosignaling cascade downstream of KRAS [1] .

Pan-KRAS-IN-6 (compound 12) is a potent pan-KRAS inhibitor, with IC50 values of 9.79 nM for Kras G12D and 6.03 nM for Kras G12V.

KRAS inhibitor-24 (compound 115c), a pyrido-pyridine class KRAS inhibitor, exhibits potent activity against KRas G12V, KRas WT, and KRas G12R, with IC50 values all below 100 nM.

K-Ras-IN-3 (compound 3) is an effective inhibitor of GDP-KRAS G12V, exhibiting an IC50 value of 0.371 nM. It has potential for use in cancer research.

KRAS inhibitor-26 (compound 194a) is an effective inhibitor of KRAS G12V (IC50: ≤100 nM), primarily utilized in cancer research.

Pan-RAS-IN-6 (compound 24) serves as a DUSP6 inhibitor, effectively reducing MAPK activation in the NCI-H1373-Luc model (DUSP6). It concurrently exhibits notable tumor growth inhibition and regression in the NSCLC brain metastasis mouse model. The compound displays high selectivity and potent inhibitory effects, particularly on KRAS mutation-associated signaling pathways. It demonstrates varied inhibitory activities against distinct KRAS mutants and their interacting proteins. The IC 50 values for KRAS G12C, G12D, and G12V are 1.3 nM, 4.7 nM, and 0.3 nM, respectively.

KRas/son of sevenless 1 (SOS1) interaction inhibitor. Binds within nucleotide binding pocket of KRas (Kd values are 106 - 176 nM for wild type KRas and various KRas mutants). Inhibits nucleotide binding to KRas in a concentration dependent manner. Display

RMC5127 is an orally available, mutation-selective RAS G12V inhibitor exhibiting central nervous system (CNS) and brain permeability. It suppresses the RAS pathway and induces apoptosis in KRAS G12V mutant cancer cells, demonstrating antitumour activity.

K-Ras-IN-1, a K-Ras inhibitor, is characterized by its chemical formula C20H19ClN4O2S and is also known as N-[(1S)-3-cyclopropyl-1-[(6-fluoro-1H-benzimidazol-2-yl)sulfanyl]-2-oxo-1-(phenylmethyl)propyl]-4-fluorobenzenesulfonamide (compound [18, dashboard 819041] in brackets).

KRAS Inhibitor-38 (Example 18) is a potent inhibitor capable of effectively suppressing the activity of KRAS G12C, KRAS G12D, and KRAS G12V in vivo.

ZZ151 is an effective and selective SOS1 PROTAC with in vivo anti-tumor efficacy against KRAS-mutant cancers. This compound induces rapid and specific degradation of SOS1 and exhibits strong anti-proliferative activity against a wide range of KRAS mutation-driven cancer cells. In murine xenograft models with KRASG12D and G12V mutations, ZZ151 demonstrates superior anticancer activity. It represents a promising lead compound for developing new chemotherapeutic agents targeting KRAS mutations.