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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.
KRAS G12C Inhibitor 68 is a selective inhibitor targeting the KRAS G12C mutation, with an IC50 of 7 nM. It exhibits significant anti-tumor activity, making it a valuable tool for cancer research, particularly in studies focused on KRAS-driven malignancies. This compound is suitable for investigating the efficacy of KRAS-targeted therapies and understanding the underlying mechanisms of KRAS-related tumorigenesis.
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CFL-120 is a potent inhibitor of the KRasG12C protein. It exhibits significant antiproliferative effects and demonstrates anticancer activity, making it a valuable tool for cancer research. CFL-120 is particularly relevant for studies focused on lung cancer therapeutics.
KRAS G12D Inhibitor 7 is a selective small molecule targeting the KRAS G12D mutation, which is commonly associated with various cancers. This compound demonstrates potent inhibitory activity against KRAS G12D-driven signaling pathways, making it a valuable tool for cancer research, particularly in studies focused on targeted therapies and drug resistance mechanisms. Its specificity for KRAS G12D highlights its potential in elucidating the role of this mutation in tumorigenesis and therapeutic response.
KRAS G12C inhibitor 42 is a selective inhibitor targeting the KRAS G12C mutation, a key driver of various cancers. This compound demonstrates significant anti-cancer activity by disrupting KRAS signaling pathways involved in tumor growth and proliferation. KRAS G12C inhibitor 42 is suitable for research applications focused on KRAS G12C-mediated malignancies and may aid in the development of targeted cancer therapies.
KRAS G12D inhibitor 16 is a selective inhibitor targeting the KRAS G12D mutation, demonstrating potent inhibitory activity with IC50 values of 0.7 nM against KRAS G12D and 0.35 μM against other KRAS G12D variants. This compound is valuable for research into various malignant tumors, including pancreatic ductal adenocarcinoma (PDAC), colon and rectal carcinomas (CRC), and non-small cell lung carcinoma (NSCLC). Its efficacy positions it as a significant tool for investigating KRAS-driven oncogenic pathways and therapeutic strategies.
SOF-436 is a selective KRAS inhibitor that targets SOS1-mediated nucleotide exchange, exhibiting an IC50 of 60 μM. Additionally, it effectively disrupts the interaction between KRAS and the effector protein RAF. This compound is primarily utilized in cancer research, providing insights into KRAS-driven oncogenic pathways.
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KRAS inhibitor-36 is a selective inhibitor targeting the KRAS Q61H mutant protein. This compound effectively interferes with KRAS signaling pathways, leading to reduced cellular proliferation and survival in KRAS-dependent cancer models. It is primarily utilized in research aimed at elucidating KRAS-related oncogenic mechanisms and developing novel therapeutic strategies for KRAS-driven malignancies.
KRAS G12C inhibitor 54 is a selective inhibitor targeting the KRAS G12C mutant protein. This compound demonstrates potent inhibition of KRAS G12C-mediated signaling pathways, leading to reduced cellular proliferation in KRAS G12C-driven tumor models. It is primarily used in cancer research, particularly for studying therapeutic strategies against KRAS G12C mutations in various malignancies.
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(S,R,S)-BBO-11818 is a selective inhibitor of KRAS, a key oncogenic driver in various cancers. This compound is instrumental in elucidating the role of KRAS in tumorigenesis and has potential applications in developing targeted therapies for KRAS-driven malignancies. It serves as a valuable tool for researchers investigating KRAS signaling pathways and their implications in cancer biology.
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pan-KRAS-IN-16 is a potent RAS inhibitor that disrupts protein-protein interactions involving RAS effector proteins. This small molecule, derived from an intracellular antibody fragment, binds to a hydrophobic pocket adjacent to the effector-binding switch regions of RAS. By inhibiting these interactions, pan-KRAS-IN-16 effectively blocks endogenous RAS-dependent signaling in tumor cell lines, making it a valuable tool for research in cancer biology and therapeutic development targeting RAS mutation-driven malignancies.
KRAS G12C Inhibitor 31 is a selective inhibitor targeting the KRAS G12C mutation, which plays a critical role in cancer pathogenesis. This compound demonstrates potent inhibitory activity, making it a valuable tool for research into KRAS-driven malignancies. It is suitable for studies focused on cancer therapeutics and mechanisms of KRAS-associated signaling pathways.
KRAS inhibitor-38 is a selective inhibitor targeting KRAS mutations, specifically KRAS G12C, KRAS G12D, and KRAS G12V. This compound effectively suppresses the activity of these mutant KRAS proteins in vivo, making it a valuable tool for research on KRAS-driven cancers. It is applicable in studies investigating the role of KRAS in tumorigenesis and potential therapeutic strategies for targeting KRAS mutations.
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KRAS G12C-IN-71 is a covalent inhibitor targeting the G12C mutation of the KRAS protein, exhibiting a Ki of 380 nM. This compound demonstrates significant biological activity by selectively inhibiting mutant KRAS, making it a valuable tool for research in non-small cell lung cancer. Its application aids in understanding the role of KRAS mutations in cancer progression and therapeutic strategies.
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KRAS G12C-IN-70 is a selective inhibitor that targets the KRAS G12C mutant, effectively disrupting downstream signaling pathways such as RAF-MEK-ERK. This inhibition leads to a reduction in tumor cell proliferation, making KRAS G12C-IN-70 a valuable tool for research into tumors associated with the KRAS G12C mutation, including non-small cell lung cancer and colorectal cancer. Researchers investigating the therapeutic potential of targeting KRAS G12C will find this compound particularly useful.
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SS-3091 is a pan KRas inhibitor that targets the interaction interfaces of KRas, leading to the destabilization of the ARaf/KRas complex and modulation of downstream signaling pathways. This compound exhibits significant anticancer and antiproliferative effects against various KRas mutant forms, including G12D, G12C, G12V, and G12S, in a range of cancer cell lines. SS-3091 is valuable for research into KRas-mediated signaling and its implications in cancer biology.
BIM-46068 is a selective inhibitor of human brain Farnesyltransferase (FTase) with an IC50 of 91.4 nM. This compound effectively inhibits Ras processing in MiaPaCa-2 cancer cells, making it a valuable tool for research on pancreatic cancer. Its ability to specifically target FTase positions BIM-46068 as an important reagent for exploring the molecular mechanisms underlying Ras signaling in cancer.
KRAS Inhibitor-17 is a selective inhibitor targeting the KRAS G12C oncogenic mutation, exhibiting an IC50 of 3.37 µM. It effectively inhibits phosphorylated ERK (p-ERK) with IC50 values of 9.25 µM in MIA PaCA-2 cells and >33.3 µM in A549 cells. This compound holds promise for advancing research in pancreatic, colorectal, and lung cancers, contributing to the understanding of KRAS-driven tumorigenesis.
DCAI is a Ras protein binder that specifically inhibits Ras activation and nucleotide exchange facilitated by SOS. This compound is valuable for studying cancer associated with mutations in the Ras gene, providing insight into the molecular mechanisms underlying Ras-driven tumorigenesis. DCAI serves as an essential tool for researchers investigating targeted therapies for Ras-related cancers.
KRAS G12C inhibitor 45 is a selective inhibitor that targets the KRAS G12C mutation, which plays a crucial role in various cancers. This compound demonstrates significant biological activity by inhibiting the downstream signaling pathways associated with KRAS G12C, thereby inducing apoptosis in tumor cells harboring this mutation. It is a valuable tool for cancer research, particularly in studies focusing on personalized medicine and targeted therapies for KRAS G12C-positive tumors.
KRAS inhibitor-21 is a potent inhibitor targeting the KRAS G12C mutation with an IC50 value of less than 0.01 μM. This compound demonstrates significant biological activity in attenuating KRAS-mediated signaling pathways, making it a valuable tool for investigating mechanisms of oncogenic transformation. It is particularly useful in cancer research aimed at exploring therapeutic strategies for KRAS-driven malignancies.
KRAS inhibitor-34 is a selective inhibitor targeting the KRAS protein, exhibiting an IC50 of 6.4 nM. This compound is utilized in tumor research to investigate KRAS-mediated signaling pathways and its role in cancer progression. It provides a valuable tool for studying the therapeutic potential of KRAS inhibition in various malignancies.
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Synonyms: (Rac)-IND 58359; (Rac)-R115777
(Rac)-Tipifarnib is a potent farnesyl protein transferase inhibitor that disrupts the post-translational modification of Ras proteins. By inhibiting farnesylation, it effectively interferes with the activation and function of Ras, leading to significant antitumor effects. This compound is utilized in research focused on cancer therapeutics and the molecular mechanisms underlying Ras-mediated signaling pathways.
PAT-IN-2 is a selective inhibitor of protein acyl transferases (PAT), primarily targeting Erf2 autopalmitoylation. By competitively inhibiting this process, PAT-IN-2 serves as a valuable tool for investigating the role of PAT in cellular signaling and lipid metabolism. Its application in research may provide insights into the regulation of protein function via acylation and the development of therapeutic strategies targeting related pathways.
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KRASG12C IN-18 is a potent covalent inhibitor targeting the KRASG12C mutation. It effectively engages KRASG12C in both GDP- and GMPPNP-bound states, demonstrating significant antiproliferative activity against KRASG12C and its resistance variants, including KRASG12C/R68S, with low nanomolar IC50 values. This compound exhibits substantial in vivo efficacy in models of KRASG12C-driven solid tumors and KRASG12C/R68S xenografts, making it a valuable tool for research in colorectal cancer.
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RAS-IN-4 is a RAS inhibitor that exhibits significant antitumor activity. This compound interferes with RAS signaling pathways, making it an important tool for researchers studying cancer biology and therapeutic resistance. RAS-IN-4 can be utilized in various in vitro and in vivo studies aimed at understanding the role of RAS in tumor progression and exploring targeted cancer therapies.
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