4 Results for "

GMPPNP

" in MedChemExpress (MCE) Product Catalog:
Products (4)

4 Results for "GMPPNP" in MCE Product Catalog:

Cat. No.: HY-W1126235
CAS No.: 2253733-45-6
Synonyms: D223
Research Areas:  

Metabolic Disease

DS02312223 (D223) is a molecular glue that promotes the binding of RAS to PI3Kα, with a Kd of 0.76 μM for p110α. DS02312223 increases the binding affinity between GTP-bound KRAS (KRAS-GMPPNP) and p110α by nearly three orders of magnitude (KD = 0.017 μM). DS02312223 stimulates the translocation of GLUT4 to the plasma membrane. DS02312223 promotes glucose uptake in the absence of insulin. DS02312223 can be used in diabetes research .
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Cat. No.: HY-179403
CAS No.: 2966924-23-0
Target:  

Ras

Research Areas:  

Cancer

KRASG12C IN-17 is an orally active covalent KRAS G12C inhibitor, showing strong inhibitory activity in KRAS G12C-mutant cancer cells (NCI-H23 IC50 = 0.7 nM; NCI-H358 IC50 = 0.5 nM). KRASG12C IN-17 covalently and irreversibly binds to KRAS G12C with > 96% modification efficiency in both GDP-bound and GMPPNP-bound conformations. KRASG12C IN-17 can be used for studies of KRAS-driven cancers, including colorectal cancer .
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Cat. No.: HY-179404
CAS No.: 2966924-24-1
Target:  

Ras

Research Areas:  

Cancer

KRASG12C IN-18 is an orally active covalent KRAS G12C inhibitor that achieves complete covalent engagement of KRAS G12C in both GDP- and GMPPNP-bound states and displays strong antiproliferative activity against KRAS G12C and resistance-associated variants, including KRAS G12C/R68S, with low-nanomolar IC50 values. KRASG12C IN-18 exhibits marked in vivo efficacy in KRAS G12C-driven solid tumor and KRAS G12C/R68S xenograft models and can be used for colorectal cancer research .
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Cat. No.: HY-181964
CAS No.: 3023465-19-9
Research Areas:  

Cancer

KRAS G12C-IN-77 is an orally active and selective KRAS G12C covalent dual-state inhibitor that binds with high affinity to both GDP-bound (inactive state) and GTP-bound (active state) KRAS G12C (IC50 = 133 nM). KRAS G12C-IN-77 rapidly inhibits ERK1/2 phosphorylation, induces the formation of covalent adducts with endogenous KRAS G12C, suppresses the expression of MAPK pathway genes, and inhibits the proliferation of KRAS G12C-mutant cells. KRAS G12C-IN-77 is applicable to research related to KRAS G12C-mutant solid tumors, including pancreatic ductal adenocarcinoma and non-small cell lung cancer .
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