kras-sos1

SOS1 KRAS-IN-1 (Compound 2) serves as an inhibitor of SOS1 KRAS, with potential application in the study of diseases mediated by SOS1 KRAS [1].

BI-3406 is an orally active, highly potent and selective between KRAS and Son of Sevenless 1 (SOS1) interaction inhibitor(IC50 : 6 nM),with anticancer activity.

BAY-293 is a potent, cell-active SOS1 inhibitor that disrupts the KRAS-SOS1 interaction (IC50: 21 nM).

SOS1 EGFR-IN-2 (Compound 4) functions as a dual inhibitor of SOS1 and EGFR, exhibiting IC50 values of 8.3 and 14.6 nM, respectively. It demonstrates significant antiproliferative effects on cancer cells harboring various KRAS mutations.

BI1701963 is an orally effective inhibitor that targets the SOS1 and KRAS interaction, specifically inhibiting the activation of KRAS by blocking its GTP loading. This compound is utilized in cancer research to explore potential therapeutic effects against KRAS-driven malignancies.

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.

BTX-6654 is a cereblon-based bifunctional SOS1 PROTAC degrader. This compound exhibits antiproliferative activity against cells with various KRAS mutations by reducing the expression of downstream signaling markers pERK and pS6.

SOS1-IN-18 (Compound 8) is an inhibitor of the Son of Sevenless 1 protein (SOS1) with a dissociation constant (KD) of 2.6 nM. It disrupts the SOS1-KRAS G12C interaction with an IC50 of 3.4 nM, inhibits ERK phosphorylation in H358 cells with an IC50 of 31 nM, and curtails the proliferation of H358 cells with an IC50 of 5 nM.

SOS1-IN-9 is a potent inhibitor of SOS1 that targets KRAS G12C-SOS1 with an IC50 of 116.5 nM.

SOS1-IN-10 is a potent inhibitor of SOS1, targeting KRAS G12C-SOS1 with an IC50 of 13 nM.

SOS1-IN-4 is a potent inhibitor of SOS1 (IC50: 56 nM) and can be used to study KRAS-C12C SOS1 interactions.

SOS1-IN-5 is a pyrimidine bicyclic derivative and a potent inhibitor of SOS1. SOS1-IN-5 interferes with the RAS-SOS1 interaction, thereby blocking KRAS activation and exhibiting broad-spectrum inhibition of KRAS activity. compound 4).

SOS1-IN-14 is a selective, potent, orally active SOS1 inhibitor (IC50: 3.9 nM). sOS1-IN-14 is absorbed in the intestine using a P-glycoprotein-mediated efflux mechanism. sOS1-IN-14 can be used in the study of KRAS mutated cancers and is more effective in tumour suppression than BI-3406.

KRAS G12C inhibitor 25 is an inhibitor of KRAS G12C. KRAS G12C inhibitor 25 inhibits the SOS1-assisted GDP GTP exchange activity of KRAS-G12C mutants with an IC50 value of 0.48 nM.

BI-0474 is a potent KRASG12C inhibitor that inhibits GDP-KRAS::SOS1 protein-protein interactions with an IC50 value of 7.0 nM.BI-0474 exhibits significant antiproliferative activity against NCI-H358 cells harboring the G12C mutation, and shows significant anti-tumor activity in a non-small cell lung cancer xenograft model. activity.BI-0474 can be used for cancer research.

KRAS G12C inhibitor 56, a powerful inhibitor of SOS1 with an inhibitory concentration (IC50) of 1.6 nM, holds promise for use in cancer research.

SOS1-IN-15 is an orally active and potent SOS1 inhibitor with potential antitumor activity.SOS1-IN-15 is used in the study of colon cancer.

PROTAC SOS1 degrader-1, a potent compound, demonstrates an effective degradation of PROTAC SOS1 with a DC50 value of 98.4 nM. It exhibits antiproliferative activity against cancer cells harboring diverse KRAS mutations and has shown an antitumor effect with low toxicity [1].

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] .

Paluratide (LUNA18) is a reversible cyclic peptide KRAS inhibitor with the advantages of oral availability and cell permeability for the treatment of kras-mutant cancers, which inhibits cancer cell proliferation by phosphorylating ERK and AKT, and also inhibits the interaction of RAS with guanine nucleotide exchange factors (GEFs).

RGT-018 is a potent oral SOS1 inhibitor with antitumor properties. It exerts its anticancer activity by inhibiting KRAS activation, thereby hindering cancer cell proliferation.

MRTX0902 is an effective and high selective inhibitor of SOS1 with an IC50 of 46 nM and a Ki of 2 nM.

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