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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.
PAT-IN-1 is a selective inhibitor of protein acyl transferases (PAT), specifically targeting Erf2 autopalmitoylation. It acts through competitive inhibition, thereby altering lipid modifications that influence protein functionality. This compound is valuable for research applications exploring the role of palmitoylation in cellular signaling and protein interactions.
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ZCL279 is a small molecule modulator that selectively inhibits the interaction between Cdc42 and intersectin (ITSN). At lower concentrations (
KRAS G12D inhibitor 13 is a selective inhibitor targeting the KRAS G12D mutation, a critical driver in various cancers. This compound effectively disrupts KRAS-mediated signaling pathways, demonstrating potent anti-cancer activity. It serves as a valuable tool for studying the role of KRAS G12D in tumor biology and evaluating potential therapeutic strategies for KRAS-related malignancies.
KRAS G12D inhibitor 9 is a selective inhibitor targeting the KRAS G12D mutant protein, a crucial element in oncogenic signaling pathways. This compound exhibits significant anti-cancer activity, making it a valuable tool for research focused on KRAS G12D-mediated tumors. Its application is vital for elucidating the mechanisms of KRAS-driven malignancies and developing targeted therapies for patients harboring this mutation.
ZG1077 is a covalent inhibitor targeting the KRAS G12C mutation. It demonstrates potent inhibitory activity against KRAS-driven cancer cell proliferation, making it a valuable tool for studying non-small cell lung cancer (NSCLC) and other KRAS-related malignancies. This compound facilitates research into therapeutic strategies aimed at inhibiting the KRAS signaling pathway.
Synonyms: Rutamycin A
Oligomycin D, an antibiotic derived from the strain S. rutgersensis, functions as a potent inhibitor of K-Ras plasma membrane localization. By disrupting K-Ras localization, Oligomycin D plays a critical role in cancer research, offering insights into tumorigenesis and potential therapeutic strategies. Its use in various cancer studies provides valuable data for understanding K-Ras-driven malignancies.
RAS-IN-5 is a potent RAS inhibitor that effectively disrupts the interaction between RAF1 and active KRAS mutant or wild-type HRAS proteins. This compound demonstrates significant inhibition of cell viability in KRAS, NRAS, and EGFR mutant cell lines. RAS-IN-5 is valuable for research applications focused on colorectal cancer, liver cancer, and non-small cell lung cancer, providing a critical tool for understanding RAS signaling and its role in tumorigenesis.
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KRAS inhibitor-11 is a potent inhibitor targeting the KRAS protein, which plays a critical role in cell signaling pathways associated with cancer proliferation. This compound exhibits significant anti-proliferative effects in KRAS-driven tumors, making it a valuable tool for cancer research. It is suitable for studies focusing on KRAS mutations and their implications in oncogenic signaling and therapeutic resistance.
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KRAS G12C Inhibitor 26 is a selective inhibitor targeting the mutant form of KRAS G12C. This compound exhibits significant antitumor activity by disrupting downstream signaling pathways associated with cell proliferation and survival. It is primarily utilized in cancer research for evaluating therapeutic strategies against KRAS-driven malignancies and understanding the role of KRAS mutations in tumorigenesis.
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KRAS G12C-IN-72 is a selective inhibitor targeting the KRAS G12C mutant protein. This compound exhibits potent activity against KRAS G12C, making it valuable for cancer research, particularly in therapeutic development. It can also serve as a ligand for synthesizing PROTACs, such as KRAS degrader-1, facilitating innovative approaches in targeted protein degradation studies.
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KRASG12D-IN-4 is a potent inhibitor of the KRAS G12D mutation, exhibiting an IC50 of 3.3 nM. This compound effectively reduces the proliferation of pancreatic cancer ASPC-1 cells, with an IC50 of 12 nM. KRASG12D-IN-4 serves as a valuable tool in cancer research, particularly for studying the therapeutic potential of targeting KRAS mutations in oncology.
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KRAS G12D-IN-34 is a potent inhibitor specifically targeting the KRAS G12D mutation, exhibiting IC50 values of 1.05 nM and 1.59 μM for KRAS G12D and wild-type KRAS, respectively. This compound is valuable for research focused on non-small cell lung cancer (NSCLC), providing insights into therapeutic strategies for KRAS-driven tumors. Its selective action enables detailed studies of KRAS-related pathways and potential treatment options.
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KRAS inhibitor-32 targets the KRAS protein, a critical component in many oncogenic signaling pathways. This compound exhibits selective inhibition of KRAS, making it a valuable tool for cancer research, particularly in the study of tumor growth and progression in KRAS-driven malignancies. Its application in preclinical studies can aid in understanding the therapeutic potential of KRAS inhibition in various cancer types.
KRAS G12C inhibitor 41 is a selective inhibitor targeting the KRAS G12C mutant protein, a critical player in oncogenic signaling pathways. This compound demonstrates significant anti-cancer activity, making it a valuable tool for investigating KRAS G12C-mediated malignancies. Its application in research can facilitate the development of targeted therapies aimed at overcoming resistance mechanisms in cancer treatment.
KRAS G12C inhibitor 53 is a selective inhibitor targeting the G12C mutated form of the KRAS protein. This compound demonstrates potent anti-proliferative activity in KRAS G12C-driven cancer cell lines, making it a valuable tool in oncology research. It is applicable for studies focused on signaling pathways involved in tumorigenesis and the development of targeted therapies for KRAS G12C mutations.
KRAS G12C Inhibitor 33 selectively targets the KRAS G12C mutant, inhibiting its activity. This compound is essential for investigating the mechanisms of KRAS-driven cancers and contributes to the development of targeted therapies. It is a valuable tool for cancer research, particularly in studies focused on signaling pathways associated with KRAS mutations.
ZINC57632462 (ACA-6) is a non-covalent allosteric inhibitor targeting KRAS. It effectively disrupts nucleotide exchange and impairs RAS-effector interaction, making it a valuable tool for investigating KRAS-related signaling pathways. This compound is particularly relevant for cancer research, enabling studies focused on tumorigenesis and therapeutic interventions.
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(±)-Spiro-oxanthromicin A is a K-Ras inhibitor with an IC50 value of 26.7 μM. This polyketide compound is derived from soil-isolated Streptomyces sp. and has been shown to mislocalize oncogenic mutant K-Ras from the plasma membrane in intact MDCK cells. (±)-Spiro-oxanthromicin A serves as a valuable tool for cancer research, particularly in studies targeting K-Ras-related pathways.
KS-58 is a K-Ras (G12D) inhibitory peptide that selectively targets and binds to K-Ras. It effectively enters cells to disrupt intracellular interactions between Ras and effector proteins. This compound demonstrates significant antitumor activity by inhibiting the proliferation of tumor cells, making it a valuable tool for research on K-Ras-related cancers and therapeutic interventions.
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KRAS-IN-5 is a selective inhibitor targeting KRAS mutants, including KRASG12D and KRASG12V, with a GNE IC50 value of 1.3 nM against KRASG12D. This compound inhibits KRAS-mediated signaling pathways, effectively blocking tumor cell proliferation by reducing ERK phosphorylation. KRAS-IN-5 exhibits potential for research applications in KRAS mutation-related cancers, including pancreatic, colorectal, and lung cancer.
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KRAS G12C inhibitor 20 is a selective inhibitor targeting the KRAS G12C mutation. This compound exhibits significant anticancer activity by disrupting KRAS signaling pathways, thereby inhibiting cellular proliferation in KRAS-dependent tumors. It is applicable in research focused on cancer biology and targeted therapies for malignancies associated with the KRAS G12C mutation.
KRAS inhibitor-26 is a potent inhibitor targeting the KRAS G12V mutation, exhibiting an IC50 of ≤100 nM. This compound effectively disrupts oncogenic signaling pathways associated with KRAS, making it a valuable tool for cancer research. Its applications include studies on tumor growth, survival, and potential therapeutic interventions in KRAS-driven malignancies.
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ZINC09659342 is an inhibitor of the Lbc-RhoA interaction, exhibiting an IC50 value of 3.6 μM. This compound serves as a valuable tool for studying RhoA-mediated cellular processes and signaling pathways. Its ability to disrupt Lbc-RhoA interactions makes it suitable for research applications in cancer biology and cellular mechanism studies.
KRAS Inhibitor-25 is a pyridopyrimidine compound that selectively inhibits KRAS with an IC50 of less than 100 nM for KRas G12V, KRas wild type (WT), and KRas G12R variants. This inhibitor is valuable for research applications focused on understanding KRAS-driven oncogenic signaling pathways and developing targeted cancer therapies. Its potency makes it suitable for studies investigating the biological effects of KRAS mutations and their role in tumorigenesis.
KRAS G12C Inhibitor 62 is designed to selectively inhibit the KRAS G12C mutant protein. This compound demonstrates potential in the study of KRAS G12C-mediated cancers, offering valuable insights into therapeutic strategies targeting this challenging oncogenic driver. Its application may facilitate research into tumor growth inhibition and the underlying mechanisms of KRAS-related malignancies.
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