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Ras inhibitors and related small GTPase modulators act on KRAS and on the Rac, Rho and Cdc42 proteins. Small GTPases of the Ras superfamily work as molecular switches. They cycle between an active form bound to guanosine triphosphate (GTP) and an inactive form bound to guanosine diphosphate (GDP). Oncogenic KRAS mutations such as G12C keep the protein in its signaling state. ARS-853 and KRas G12C inhibitor 4 target the mutant cysteine of KRAS G12C, while Kobe2602 interferes with binding of Ras to Raf. Salirasib, a farnesylcysteine mimetic, disrupts the membrane association of Ras. Rho-family tools include NSC 23766 and EHT 1864, which inhibit Rac, and CASIN, which targets Cdc42.
pan-KRAS-IN-15 is a pan-KRAS inhibitor that targets multiple KRAS mutant variants. This compound exhibits potent inhibitory activity against KRAS-driven signaling pathways, making it valuable for studying the mechanisms of KRAS-related cancers. It is particularly relevant for research focused on pancreatic cancer, providing insights into therapeutic strategies and disease progression.
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KRAS Inhibitor-22 is a selective inhibitor of the K-Ras protein, specifically targeting the Kras 4B(G12D) and Kras 4B(G12C) mutant forms. This compound exhibits potent anti-cancer activity, making it a valuable tool in cancer research aimed at understanding K-Ras-driven malignancies. Its application can aid in elucidating the role of K-Ras in cancer progression and therapeutic resistance.
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KRAS inhibitor-13 is a selective inhibitor targeting the mutant KRAS G12C protein, demonstrating its potency with an IC50 value of 0.883 µM. This compound effectively inhibits phosphorylated ERK (p-ERK) in cell lines, showing IC50s of 5.9 µM in MIA PaCA-2 cells and >100 µM in A549 cells. KRAS inhibitor-13 is poised for research applications focused on pancreatic, colorectal, and lung cancers, providing insights into therapeutic strategies against KRAS-driven malignancies.
KRAS G12C Inhibitor 44 is a potent and orally bioavailable inhibitor targeting the KRAS G12C mutation. This compound exhibits significant anti-proliferative activity, with IC50 values of 0.016 µM in MIA PaCA-2 cells and 0.028 µM in H358 cells. Additionally, KRAS G12C Inhibitor 44 demonstrates antitumor effects in vivo, making it a valuable tool for cancer research focusing on KRAS-driven malignancies.
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KRAS G12C inhibitor 52 is a selective inhibitor targeting the KRAS G12C mutant protein. This compound effectively disrupts KRAS signaling pathways, thereby inhibiting cell proliferation and survival in KRAS G12C-driven cancers. Its research applications include studies on cancer biology, drug development, and understanding resistance mechanisms in targeted therapies.
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KRAS inhibitor-12 is a potent inhibitor specifically targeting the KRAS G12C mutation, exhibiting an IC50 of 0.537 µM. This compound demonstrates effective inhibition of phosphorylated ERK in MIA PaCA-2 and A549 cells, with IC50 values of 1.3 µM and 3.7 µM, respectively. KRAS inhibitor-12 is a valuable tool for investigating therapeutic strategies in pancreatic, colorectal, and lung cancers.
KRAS G12D inhibitor 12 specifically targets the KRAS G12D mutation, a critical player in cellular signaling pathways associated with tumorigenesis. This compound exhibits potent anti-cancer activity, making it a valuable tool for researchers investigating KRAS G12D-mediated cancers. Its application includes evaluating therapeutic strategies and understanding the molecular mechanisms of oncogenic signaling in various cancer types.
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KRAS G12C Inhibitor 46 is a potent inhibitor targeting the KRAS G12C mutation, an essential driver in various cancers. This compound effectively blocks the aberrant signaling pathways associated with KRAS G12C, leading to reduced proliferation and enhanced apoptosis in cancer cells harboring this mutation. It is primarily utilized in cancer research, particularly for exploring therapeutic strategies targeting KRAS-dependent tumors.
KRAS Inhibitor-23 is a selective inhibitor targeting KRAS, a critical protein involved in cell signaling pathways that regulate cell growth and differentiation. This compound demonstrates significant biological activity by effectively disrupting KRAS-mediated oncogenic signaling, making it a valuable tool in cancer research. Its application spans the investigation of KRAS mutations and their role in tumor progression, providing insights into potential therapeutic strategies for KRAS-driven malignancies.
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KRASG12D-IN-5 is a potent inhibitor targeting the KRAS(G12D) mutation, exhibiting an IC50 of 11 nM. This compound demonstrates significant anticancer activity, displaying low cytotoxicity against various cell lines, including 10.37 μM for BxPC-3 (wild type), 0.76 μM for KRAS mutant AsPC-1 (G12D), and 0.3 μM for MIAPaCa-2 (G12C). KRASG12D-IN-5 is valuable for cancer research, particularly in the context of lung, pancreatic, and colorectal cancers.
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KRAS-IN-48 free base is a highly selective inhibitor targeting mutant KRAS, specifically KRAS G12D and KRAS G12V, with Kd values of 2.58 nM and 5.49 μM, respectively. This compound effectively reduces pERK expression in KRAS-mutant cells, exhibiting IC50 values of 1.1 μM and 1.51 μM for KRAS G12D and G12V mutations. KRAS-IN-48 free base serves as a valuable tool in cancer research, contributing to the understanding of KRAS-driven malignancies.
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KRAS G12D inhibitor 24 is a potent inhibitor of the KRAS G12D mutant, exhibiting an IC50 of 0.004 μM. This compound demonstrates significant oral bioactivity, making it suitable for in vivo studies. Its primary applications include exploring therapeutic avenues in cancer research, specifically for tumors driven by KRAS G12D mutations.
KRAS G12C inhibitor 58 specifically targets the KRAS G12C mutant protein, effectively disrupting its activity and downstream signaling pathways. This compound demonstrates potent antitumor efficacy, making it a valuable tool for studying KRAS-driven malignancies. Its applications extend to cancer research, particularly in the development and testing of novel therapeutic strategies for treating KRAS G12C-dependent tumors.
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pan-KRAS-IN-13 is a potent KRAS inhibitor that targets mutant forms of the KRAS protein, demonstrating IC50 values of 2.75 nM and 2.89 nM for G12D and G12V mutations, respectively. This compound is valuable for research applications aimed at understanding KRAS-driven cancers and evaluating therapeutic strategies to inhibit KRAS signaling pathways. Its high specificity and efficacy make it a critical tool for the study of oncogenic mutations associated with various malignancies.
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RNK08954 is a KRAS G12D inhibitor targeting the KRAS oncogene mutation commonly found in various cancers. This compound demonstrates the ability to impede KRAS-driven cellular signaling pathways, making it a valuable tool for investigating the role of KRAS G12D in tumorigenesis. RNK08954 is suitable for research applications focused on cancer biology and therapeutic development against KRAS-mutant tumors.
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8-Br-2'-O-Me-cAMP is a synthetic analog of cyclic AMP (cAMP) that selectively activates exchange factors activated by cAMP (Epac) without stimulating protein kinase A (PKA). This unique property makes it a valuable tool for investigating cAMP-mediated signaling pathways. It is particularly relevant in studies related to cardiovascular diseases, facilitating the exploration of Epac's role in cardiac function and pathology.
KRAS G12C inhibitor 40 is a selective inhibitor targeting the KRAS G12C mutation, a critical driver in various cancers. This compound disrupts the aberrant signaling pathways associated with KRAS G12C, demonstrating significant anti-cancer activity. KRAS G12C inhibitor 40 is valuable for research into the mechanisms of KRAS G12C-mediated tumorigenesis and for the development of targeted cancer therapies.
ARS-2102 is a potent covalent inhibitor of the KRAS G12C mutation, a key driver in various cancers. By selectively targeting this mutated oncogene, ARS-2102 exhibits significant anti-tumor activity, making it a valuable tool for cancer research. Its application is particularly relevant in studies focused on therapeutic strategies for KRAS-driven malignancies.
NSC 1008 is a selective inhibitor of Ras converting enzyme 1 (Rce1), exhibiting an in vitro IC50 of 8.9 μM in human cells. This compound demonstrates specificity for Rce1, showing minimal inhibitory effects on human Ste24 and farnesyltransferase. NSC 1008 has low cellular toxicity and effectively induces mislocalization of EGFP-Ras from the plasma membrane in cancer cells. It serves as a valuable reagent for cancer research, facilitating studies on Rce1's role in oncogenic signaling pathways.
Synonyms: APY-606; Clospirazine hydrochloride
Spiclomazine hydrochloride is a KRas inhibitor recognized for its dual role as an antipsychotic and antitumor agent. This compound effectively induces apoptosis in cancer cells, making it a valuable tool in cancer research. Its action on KRas allows for exploration into the mechanisms of tumorigenesis and potential therapeutic strategies targeting KRas-driven malignancies.
RAS Activator Compound 1 is a specific activator targeting the guanine nucleotide exchange factor, son of sevenless homologue 1 (SOS1). This compound effectively facilitates the nucleotide exchange process, leading to increased levels of active RAS-GTP in HeLa cells. RAS Activator Compound 1 is valuable for research focused on RAS-driven tumors, providing insights into the mechanisms of RAS activation and its role in cancer biology.
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KRAS G12C inhibitor 39 is a selective inhibitor targeting the KRAS G12C mutation, which is frequently associated with various cancers. This compound demonstrates significant anti-tumor activity by interfering with KRAS signaling pathways, making it a valuable tool for research into KRAS G12C-mediated oncogenesis. Its application extends to studies aimed at understanding the efficacy of targeted therapies in KRAS-driven malignancies.
AMG410 diTFA is a selective pan-KRAS inhibitor targeting various KRAS mutations, including G12D, G12V, and G13D, with IC50 values ranging from 1 to 4 nM. It exhibits over 100-fold selectivity against HRAS and NRAS and acts as a dual inhibitor of GTP-bound and GDP-bound states (Kd(GDP) of 1 nM; Kd(GTP) of 22 nM). AMG410 diTFA effectively disrupts KRAS signaling irrespective of cycling state and inhibits proliferation in wild-type KRAS-amplified tumor cells. This compound is valuable for research on colorectal, pancreatic, and lung cancers.
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KRAS G12C Inhibitor 47 is a selective inhibitor targeting the KRAS G12C mutation, exhibiting an IC50 of 0.172 µM. It effectively inhibits p-ERK signaling, with IC50 values of 0.046 µM in MIA PaCA-2 cells and 69.8 µM in A549 cells. This compound is a valuable tool for researching therapeutic strategies in pancreatic, colorectal, and lung cancers.
KRAS Inhibitor-15 is a selective inhibitor targeting the KRAS G12C mutation, exhibiting a potent IC50 of 0.954 µM. This compound demonstrates effective inhibition of phosphorylated ERK (p-ERK) with IC50 values of 2.03 µM in MIA PaCA-2 cells and >33.3 µM in A549 cells. KRAS Inhibitor-15 is suitable for investigating therapeutic strategies in pancreatic, colorectal, and lung cancers, contributing to the understanding of KRAS-driven tumorigenesis.
