ACA-14 is a small molecule direct inhibitor of KRAS, impedes the interaction of KRAS with its effector Raf and reduces both intrinsic and SOS-mediated nucleotide exchange rates.

AMG410 is a non-covalent and selective pan-KRAS inhibitor with IC50 values of 1-4 nM for KRAS G12D, KRAS G12V, and KRAS G13D. AMG410 shows greater than 100-fold selectivity against both HRAS and NRAS. AMG410 is a dual GTP(on)- and GDP(off)-state inhibitor (Kd(GDP-state) of 1 nM; Kd(GTP-state) of 22 nM). AMG410 blocks KRAS signaling in a cycling state-independent manner and also blocks proliferation in wildtype KRAS-amplified tumor cells. AMG410 can be used for the study of colorectal, pancreatic, and lung cancers.

KRAS inhibitor-42 (compound 8) is a potent USP7 inhibitor. KRAS inhibitor-42 has high affinity against GDP-bound KRASG12D with a Ki of 2.7 μM.

ADT-1004 is an inhibitor of RAS. ADT-1004 can be studied in research for Ras-mediated diseases.

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 Kds 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 KRASG12C 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.

Z56 is a Ras protein inhibitor. Z56 can be used for the research of cancer, such as pancreatic cancer.

Z52 is a Ras protein inhibitor. Z52 can be used for the research of cancer, such as pancreatic cancer.

Z52-L16 is Drug-Linker Conjugates for ADC, which is composed of a linker and a Ras inhibitor Z52. Z52-L16 can be used for the research of cancer, such as pancreatic cancer.

(S)-AZD0022 is an isomer of AZD0022, AZD0022 is a selective and orally active KRASG12D inhibitor. AZD0022 inhibits KRAS pathway suppression in the GP2D xenograft model.

SHY-855 is a pan RAS inhibitor. SHY-855 effectively prevents the binding of K-Ras proteins and other members of the Ras superfamily of small GTPases with IC50 values of 0.3-5 μM. SHY-855 effectively inhibits the phosphorylation of MEK, ERK1/2, and AKT downstream of K-Ras. SHY-855 inhibits the formation of the Ras-GTP activity complex. SHY-855 can be used to the studies of pancreatic cancer and non-small cell lung cancer.

SHY-867 is a pan RAS inhibitor. SHY-867 effectively prevents the binding of K-Ras proteins and other members of the Ras superfamily of small GTPases with EC50 values of 0.5-3 μM. SHY-867 effectively inhibits the phosphorylation of MEK, ERK1/2, and AKT downstream of K-Ras. SHY-867 inhibits the formation of the Ras-GTP activity complex. SHY-867 can be used to the studies of pancreatic cancer and non-small cell lung cancer.

(R)-KRAS G12D inhibitor 28 hydrochloride dehydrate is the hydrochloride dehydrate of (R)-KRAS G12D inhibitor 28. KRAS G12D inhibitor 28 (Compound 1) is a KRAS G12D inhibitor. KRAS G12D inhibitor 28 (Compound 1) can be used in the cancer research.

VVD-849 is a RAS ligand. VVD-849 binds covalently to cysteine 242 in the RAS binding domain of PI3K p110α and promotes RAS/PI3K interaction. VVD-849 partially inhibits pAKT(S473) in HER2 over-expressing tumors. VVD-849 can be used cancers like breast cancer research.

AH001 is a orally active RhoA inhibitor, which binds a cryptic pocket proximate to GDP within RhoA with a KD of 73.16 nM. AH001 interacts with GDP, stabilizing RhoA’s interaction with its endogenous inhibitor, RhoGDIα. AH001 reduces the downstream MRTFA nuclear translocation and downregulates fibrosis/hypertrophy proteins. AH001 mitigates myocardial remodeling in multiple HF animal models, and in the 3D myocardial tissue model. AH001 exerts its cardioprotective effects through the RhoA-RhoGDIα axis, effectively inhibiting downstream RhoA activation signaling.

(±)-Spiro-oxanthromicin A (Compound 4), a polyketide, is a K-Ras inhibitor with an IC50 of 26.7  μM. (±)-Spiro-oxanthromicin A can be isolated from soil-derived Streptomyces sp. (±)-Spiro-oxanthromicin A can mislocalize oncogenic mutant K-Ras from the plasma membrane of intact MDCK cells. (±)-Spiro-oxanthromicin A can be used for cancers research.

Z52/Z56 intermediate is a key intermediate in the synthesis of RAS inhibitors.

VVD-442 is a covalent RAS-PI3K inhibitor. VVD-442 binds covalently to cysteine 242 in the RAS binding domain of PI3K p110α and blocks RAS/PI3K interaction. VVD-442 can be used cancers like breast cancer research.

Scrambled Tadnersen is the Negative Control of Tadnersen sodium. Tadnersen sodium, an antisense oligonucleotide (ASO), selectively targets C9ORF72 transcript variants 1 and 3 that carry the expansion.

Scrambled Tadnersen sodium is the Negative Control of Tadnersen sodium. Tadnersen sodium, an antisense oligonucleotide (ASO), selectively targets C9ORF72 transcript variants 1 and 3 that carry the expansion.

Calderasib (MK-1084) is a selective KRAS G12C inhibitor demonstrating antitumor efficacy. It can be utilized as monotherapy or in combination with pembrolizumab () for oncology research.

RMC5127 is a first-in-class, orally bioavailable mutant-selective tri-complex inhibitor of the GTP-bound (ON) form of RASG12V. It non-covalently binds to cyclophilin A (CypA), forming a binary complex that engages RASG12V(ON) to form a high-affinity tri-complex, sterically inhibiting RAS binding. It inhibits the RAS pathway in KRASG12V-mutant cancer cells, reducing proliferation, inducing apoptosis, and showing strong potential for use in RASG12V-mutated cancer research.

ZCL279 is a small molecule modulator (SMM) that inhibits Cdc42-intersectin (ITSN) interaction. ZCL279 can activate Cdc42 (a cytoplasmic small GTPase in the Ras superfamily) at lower concentrations (<10 μM) and significantly inhibit it at higher concentrations (<10 μM).

VVD-699 is a covalent RAS-PI3K inhibitor. VVD-699 covalently binds to cysteine 242 in the RAS binding domain of PI3K p110α, thereby blocking the ability of RAS to activate PI3K activity. VVD-699 is able to inhibit the growth of RAS-mutated and HER2-overexpressing tumors. VVD-699 can be used to study cancers associated with RAS mutations (e.g., H358 lung cancer cells, A549 cells, FaDu cells).

Sosimerasib is the inhibitor for kirsten rat sarcoma viral oncogene homolog (KRAS) and exhibits antineoplastic activity.

SOF-436 is a KRAS inhibitor that inhibits SOS1-mediated KRAS nucleotide exchange (IC50 = 60 μM) and the binding of KRAS to the effector protein RAF. SOF-436 can be used in cancer research.

RMC-5127 is an orally active and brain-penetrant mutant-selective tri-complex RASG12V inhibitor. RMC-5127 non-covalently binds to cyclophilin A (CypA), forming a binary complex that engages RASG12V(ON) to form a high-affinity tri-complex, sterically inhibiting RAS binding . RMC-5127 inhibits the RAS pathway in KRASG12V mutant cancer cells, reducing cell proliferation and inducing apoptosis. RMC-5127 is promising for research of cancers with RAS mutations, such as non-small cell lung cancer.

RMC-4998 formic is an orally active inhibitor targeting the active or GTP-bound state of the KRASG12C mutant. RMC-4998 formic can form a ternary complex with intracellular CYPA and the activated KRASG12C mutant, with an IC50 value of 28 nM. RMC-4998 formic can inhibit ERK signaling in KRASG12C mutant cancer cells and induce apoptosis. RMC-4998 formic can be used for tumor research.

KRASG12C IN-16 (Compound SK-17) is a selective, covalent and an orally active KRASG12C inhibitor. KRASG12C IN-16 induces Apoptosis. KRASG12C IN-16 effectively prevents the activation of MAPK and PI3K/mTOR signaling pathways. KRASG12C IN-16 displays anti-tumor activity against pancreatic cancer.

KRASG12C IN-15 (Compound 21) is the orally active inhibitor for KRASG12C, and inhibits SOS1-mediated GDP/GTP exchange with an IC50 of 19 nM. KRASG12C IN-15 inhibits the phosphorylation of ERK with IC50 of 0.051 μM. KRASG12C IN-15 inhibits the cell viability of KRASG12C mutated MIA PaCa-2 with IC50 of 0.023 μM. KRASG12C IN-15 exhibits antitumor effect in MIA PaCa-2 xenograft mouse models.

INCB159020 is an orally active KRAS G12D inhibitor with a KRAS G12D SPR value of 2.2 nM. INCB159020 has antitumor activity.