2. GPCR/G Protein MAPK/ERK Pathway
  3. Ras
  4. KRAS G12C inhibitor 57

KRAS G12C inhibitor 57 (Compound 50) is a potent, selective, covalent and orally active KRAS G12C inhibitor with an IC50 of 0.21 μM in KRAS G12C/SOS1 binding assay. KRAS G12C inhibitor 57 induces cancer cell apoptosis.

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KRAS G12C inhibitor 57 Chemical Structure

KRAS G12C inhibitor 57 Chemical Structure

CAS No. : 2821863-70-9

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KRAS G12C inhibitor 57 Related Antibodies

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Description

KRAS G12C inhibitor 57 (Compound 50) is a potent, selective, covalent and orally active KRAS G12C inhibitor with an IC50 of 0.21 μM in KRAS G12C/SOS1 binding assay. KRAS G12C inhibitor 57 induces cancer cell apoptosis[1].

IC50 & Target[1]

KRAS(G12C)

0.21 μM (IC50, KRAS G12C/SOS1 binding assay)

In Vitro

KRAS G12C inhibitor 57 (Compound 50) (0-10 μM; 3 days) has selective inhibition on KRAS and KRAS-driven cell lines, together with strong inhibition on downstream signaling[1].
KRAS G12C inhibitor 57 (0.1-1 μM; 24 h) induces H358 cell apoptosis[1].
KRAS G12C inhibitor 57 (0.1-1 μM; 48 h) inhibits tumor metastasis in H358 cells[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

KRAS G12C inhibitor 57 Related Antibodies

Western Blot Analysis[1]

Cell Line: H358 (KRAS p. G12C) cells
Concentration: 0, 0.1, 0.3, 0.5, 1 and 5 μM
Incubation Time: 4 and 24 h
Result: Inhibited the active KRAS-GTP and the phosphorylation of ERK and AKT (MAPK and PI3K pathway) in the dose- and time-dependent manners, and strong inhibitory effects on the phosphorylation of ERK at the concentration of 0.1 μM. Increased the cleaved PARP and caspase-7 induction (24 h).

Western Blot Analysis[1]

Cell Line: H1975 cell line
Concentration: 5, 10, and 20 μM
Incubation Time: 4 h
Result: Interrupted the phosphorylation of ERK.

Cell Proliferation Assay[1]

Cell Line: H358 cells harboring KRAS p.G12C, MIA Paca2 cells harboring KRAS p.G12C, H1975 cells harboring KRAS p.WT and A549 cells harboring KRAS p.G12S
Concentration: 0-10 μM
Incubation Time: 3 days
Result: Displayed favourable inhibitory activities on H358 cells and MIA Paca2 cells with the IC50 values of 0.16 μM and 0.87 μM, in sharp contrast with no obvious inhibition on cell proliferation on H1975 cells (IC50 = 7.91 μM) and A549 cells (IC50 = 29.9 μM).

Apoptosis Analysis[1]

Cell Line: H358 cell line
Concentration: 0.1, 0.3, 0.5 and 1 μM
Incubation Time: 24 h
Result: Induced cellular apoptosis in dose-dependent manner.

Cell Migration Assay [1]

Cell Line: H358 cells
Concentration: 0.1, 0.5 and 1 μM
Incubation Time: 48 h
Result: Significantly suppressed the migration.

Cell Invasion Assay[1]

Cell Line: H358 cells
Concentration: 0.1, 0.5 and 1 μM
Incubation Time: 48 h
Result: Inhibited the cellular invasion and exhibited the dose-dependent inhibitory potency.
In Vivo

KRAS G12C inhibitor 57 (Compound 50) (10 and 30 mg/kg; p.o.; daily for 20 days) shows anti-tumor efficacy in mice H358 xenograft model[1].
Pharmacokinetic data of KRAS G12C inhibitor 57 (Compound 50) in ICR mice. [1]

Parameter iv (3 mg/kg) Parameter po (30 mg/kg)
AUC(0−t) (h*ng/mL) 801 AUC(0−t) (h*ng/mL) 600
AUC(0−∞) (h*ng/mL) 804 AUC(0−∞) (h*ng/mL) 835
C0 (ng/mL) 1964 Cmax (ng/mL) 316
T1/2 (h) 0.930 T1/2 (h) 4.79
Vss (L/kg) 4.98 Tmax (h) 0.083
CL (mL/h/kg) 3739 F (%) 10.4
AUCo‑inf (h*mg/mL) 7060 ± 1020 (14.5%) 21800 ± 2310 (10.6%) 101000 ± 16700 (16.6%)

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: BALB/c-nu/nu mice, H358 xenograft model[1]
Dosage: 10 mg/kg and 30 mg/kg
Administration: Oral administration, daily for 20 days
Result: Significantly inhibited the tumor growth in a dose-dependent manner with remarkable tumor regression at the dose of 30 mg/kg (tumor growth inhibition, TGI = 84.0%). All dosage groups were well-tolerated with no loss of body weight and no morphological damage to viscera including the heart, spleen, and kidney. Significantly suppressed the phosphorylation of ERK and AKT in tumors of nude mice when dosing orally at 10 mg/kg and 30 mg/kg.
Animal Model: ICR mice[1]
Dosage: 3 mg/kg or 30 mg/kg
Administration: IV or PO (Pharmacokinetic Analysis)
Result: Displayed reasonable clearance and half-life by iv administration. Showed a moderate oral bioavailability (F) of 10.4%.
Molecular Weight

607.72

Formula

C35H38FN7O2
CAS No.
SMILES

N#CC[C@@H]1N(C(C=C)=O)CCN(C2=C3C(N(C)C(C4=C5C(C)=CC=CC5=CC=C4)=C3)=NC(OC[C@@]67CCCN6C[C@H](F)C7)=N2)C1
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KRAS G12C inhibitor 57 Related Classifications

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Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

KRAS G12C inhibitor 572821863-70-9RasH358H1975MIA Paca2A549BALB/c-nu/nu miceanticancerInhibitorinhibitorinhibit

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