Ras Inhibitor

Sosimerasib is an orally active KRAS^G12C inhibitor. Sosimerasib can be used in research related to non-small cell lung cancer.

MRTX-EX185 formic is a potent KRAS (G12D) inhibitor with an IC₅₀ of 90 nM. MRTX-EX185 formic can binds both GDP-loaded and active GNP states of KRAS and KRAS (G12D). MRTX-EX185 formic exhibits broad-spectrum binding properties with IC₅₀s of 110, 290, 130 and 240 nM for KRAS WT, KRAS (G12C), KRAS (Q61H), KRAS (G13D). MRTX-EX185 formic also binds GDP-loaded HRAS. MRTX-EX185 formic can be used to study various RAS-driven tumors (such as pancreatic cancer) .

SOS1-IN-14 is a potent, selective and orally active SOS1 inhibitor with an IC₅₀ value of 3.9 nM. SOS1-IN-14 can be absorbed in the intestine via a P-glycoprotein-mediated efflux mechanism. SOS1-IN-14 can be used to research KRAS-mutated cancers. SOS1-IN-14 has better potent tumor suppression than BI-3406 (HY-125817).

MM41 is a quadruplex-interacting compound. MM41 binds tightly to quadruplexes encoded in the promoter sequences of the BCL-2 and k-RAS genes. MM41 reduces BCL-2 and k-RAS protein levels, increases caspase 3. MM41 has antitumor effects against pancreatic cancer.

RBC6 is an inhibitor of GTPases RalA. RBC6 inhibits binding of Ral to its effector RALBP1. RBC6 also inhibits Ral-mediated cell spreading of murine embryonic fibroblasts, as well as anchorage-independent growth of human cancer celllines.

RSC-1255 is a potent and selective Vacuolar H⁺-ATPase (V-ATPase) inhibitor that directly binds the mammalian V-ATPase complex with a K_d = 23 nM. RSC-1255 exhibits preferential cytotoxicity toward KRAS-mutant cancer cells, especially KRAS^G13D and KRAS^G12V cells. RSC-1255 induces apoptosis and blocks lysosomal acidification, autophagy, and macropinocytosis in cancer cells. RSC-1255 can be used for the study of KRAS-driven lung and colon cancers.

CMC2.24 (TRB-N0224), an orally active tricarbonylmethane agent, is effective against pancreatic tumor in mice by inhibiting Ras activation and its downstream effector ERK1/2 pathway. CMC2.24 is also a potent inhibitor of zinc-dependent MMPs with IC₅₀s ranging from 2.0-69 μM. CMC2.24 alleviates osteoarthritis progression by restoring cartilage homeostasis and inhibiting chondrocyte apoptosis via the NF-κB/HIF-2α axis.

KRAS G12C inhibitor 67 (Example 35) is an orally active KRAS G12C inhibitor. KRAS G12C inhibitor 67 inhibits pERK and active KRas. KRAS G12C inhibitor 67 selectively inhibits the growth of various KRAS G12C mutant tumor cell lines. KRAS G12C inhibitor 67 exhibits anticancer activity against esophageal cancer, bladder cancer, colorectal cancer, lung cancer, and pancreatic cancer.

I194496 is a potent cystathionine γ-lyase (CSE) inhibitor, with an IC₅₀ of 0.79 mM. I194496 can inhibit the growth of human TNBC cells via the dual targeting PI3K/Akt and Ras/Raf/ERK pathway and suppress the metastasis of human TNBC cells via down-regulating Anxa2/STAT3 and VEGF/FAK/Paxillin signaling pathways.

EPAC 5376753, a 2-Thiobarbituric acid (HY-77962) derivative, is a selective and allosteric Epac inhibitor. EPAC 5376753 inhibits Epac1 with an IC₅₀ of 4 µM in Swiss 3T3 cells. EPAC 5376753 does not inhibit PKA and adenylyl cyclases.

TH-Z827 is a selective KRAS^G12D inhibitor that exhibits activity against GDP-bound and GMPPNP-bound KRAS^G12D, but shows no activity against KRAS (WT) and KRAS^G12C. TH-Z827 blocks the KRAS^G12D-CRAF interaction with a IC₅₀ value of 42 μM. TH-Z827 can be used for the research of pancreatic cancer.

(E/Z)-ZINC09659342 is an inhibitor of Lbc-RhoA interaction.

Fendiline (hydrochloride) (Standard) is the analytical standard of Fendiline (hydrochloride). This product is intended for research and analytical applications. Fendiline hydrochloride, a diphenylalkylamine type of antianginal agent, is an L-type calcium channel blocker (IC50 of 17 µM). Fendiline hydrochloride is also a selective K-Ras inhibitor, and has no effect on H-Ras and N-Ras. Fendiline hydrochloride inhibits K-Ras plasma membrane localization (IC50 of 9.64 μM), inhibits K-Ras signal output and blocks the proliferation of pancreatic, colon, lung, and endometrial cancer cell lines expressing oncogenic mutant K-Ras. Fendiline hydrochloride is a STING agonist and is able to inhibit the growth of multiple refractory cold tumors (MC38, CT26 and B16F10).

MCB-294 is a dual-state pan-KRAS inhibitor that selectively inhibits KRAS over NRAS and HRAS. MCB-294 capable of binding both the active (GTP-bound) and inactive (GDP-bound) forms of KRAS with K_ds of approximately 1 pM and 10 nM, respectively. MCB-294 broadly impairs the growth of hTERT-HPNE cells expressing G12D, G12C, G12V, G12S, G13D, and wild-type KRAS, with IC₅₀s of approximately 700 nM. MCB-294 induces irreversible apoptosis in KRAS-mutated tumors. MCB-294 effectively suppress KRAS^G12C inhibitor-resistant cancer cells and remodel the tumor immune microenvironment. MCB-294 can be used for the study of pancreatic cancer, colorectal cancer and lung cancer.

RGT-018 is a potent and orally active SOS1 inhibitor with anti-tumor effects. RGT-018 exerts anti-cancer cell proliferation activity by inhibiting KRAS activation.

INCB159020 is an orally active KRAS^G12D inhibitor with equivalent binding potency for the active GTP-bound and inactive GDP-bound forms of KRAS^G12D. INCB159020 can be used in the research of KRAS-driven cancers.

RM-018 is a potent, functionally distinct tricomplex KRAS^G12C active-state inhibitor. RM-018 retains the ability to bind and inhibit KRAS^G12C/Y96D and could overcome resistance. RM-018 binds specifically to the GTP-bound, active [“RAS(ON)”] state of KRAS^G12C.

ASP2453 is a potent, selective and orally active KRAS G12C inhibitor. ASP2453 inhibits the Son of Sevenless (SOS)-mediated interaction between KRAS G12C and Raf with an IC₅₀ value of 40 nM.

SOS1-IN-11 is a potent SOS1 inhibitor with an IC₅₀ value of 30 nM.

KRAS G12D inhibitor 14 is a potent KRAS G12D inhibitor with a K_D of 33 nM for binding to KRAS G12D protein. KRAS G12D inhibitor 14 decreases the active form of KRAS G12D (KRAS G12D-GTP) but not KRAS G13D.