gtp-kras

KRAS inhibitor-9 (DUN09716) is a potent KRAS inhibitor with Kd of 92 μM that blocks the formation of GTP-KRAS and downstream activation of KRAS. KRAS inhibitor-9 causes G2/M cell cycle arrest and induces apoptosis. KRAS inhibitor-9 selectively inhibits the proliferation of NSC-LC cells with KRAS mutation but not normal lung cells

RMC-7977 is a highly selective inhibitor of the active (GTP-bound) forms of KRAS, HRAS, and NRAS with anticancer activity for the study of solid tumors with KRAS G12C mutations.

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.

AMG410 is a non-covalent, dual-modality KRAS inhibitor effective against both GDP (OFF) and GTP (ON) binding, with Kd (GDP) of 1 nM and Kd (GTP) of 22 nM, capable of blocking KRAS independently of the cell cycle. AMG410 does not affect HRAS and NRAS2, and exhibits high potency against KRAS G12D, G12V, G12C, G13D, and other mutants, with an IC₅₀ of 1–4 nM. It induces tumour regression and reduces phosphorylated ERK levels in KRAS-mutant cancer models.

RMC5127 is an oral and mutation-selective inhibitor of RASG12V (ON) that inhibits the GTP-bound (ON) form of RAS G12V through the formation of a high-affinity triplex with central nervous system (CNS) permeability and brain permeability. RMC5127 inhibits RAS pathway activity in vitro in KRAS G12V mutant human cancer cells and cellular proliferation, and antitumor activity in preclinical intracranial xenograft models and subcutaneous CDX and PDX models of KRAS G12V mutant NSCLC, PDAC and CRC.

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.

RAS RAS-RAF-IN-1 is a potent inhibitor of RAS and RAS-RAF, exhibiting a KD of 5.0 μμ-15 μμ for cyclophilin A (CYPA) binding affinity and demonstrating antitumor activity[1].

KRA-533, a potent KRAS agonist, directly targets the GTP/GDP binding pocket within the KRAS protein, inhibiting GTP cleavage. This inhibition leads to the buildup of constitutively active GTP-bound KRAS, which subsequently activates both apoptotic and autophagic cell death pathways specifically in cancer cells.

KRAS G12D inhibitor 14 is a potent compound that binds the KRAS G12D protein (Kd: 33 nM) and selectively inhibits the active form KRAS G12D-GTP, but not KRAS G13D.

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.

ARS-853 is an inhibitor of K-RASG12C(IC50 : 2.5 μM), a mutant form of K-RAS that accumulates in the active GTP-bound state in certain cancer cells

AZD4747 is a selective and potent inhibitor of the mutant GTPase KRASG12C that crosses the blood-brain barrier and has potential antitumor activity for the study of pancreatic and colorectal adenocarcinoma.

BBO-8520 is an orally available direct small molecule covalent inhibitor that targets KRAS G12C. It functions as a KRAS G12C (OFF) inhibitor and blocks the KRAS G12C (ON) signal by binding to the GTP protein, thereby inhibiting cell proliferation. Additionally, BBO-8520 can disrupt the RAS-RAF1 interaction, returning KRAS G12C to its inactive (OFF) state [1].

BC-LI-0186 (4-(2,3-dimethyl-5-oxo-4-propan-2-ylpyrazol-1-yl)-N-(2-phenoxyethyl)benzenesulfonamide) is a potent and selective inhibitor of the interaction of Leucyl-tRNA synthetase (LRS) and Ras-related GTP-binding protein D (RagD) with IC50 of 46.11 nM. BC-LI-0186 competitively binds the RagD interaction site of LRS with Kd of 42.1 nM and has no effect on LRS-vps34, LRS-eprs, RagB-RagD association, mTORC1 complex formation. BC-LI-0186 potently inhibits the activity of tumor-associated MTOR mutants and the growth of rapamycin-resistant cancer cells. BC-LI-0186 can be used for lung cancer-related research.