9 Results for "

AKT-IN-5

" in MedChemExpress (MCE) Product Catalog:
Products (9)

9 Results for "AKT-IN-5" in MCE Product Catalog:

Cat. No.: HY-138767
CAS No.: 1402608-05-2
Target:  

Akt

Research Areas:  

Cancer

AKT-IN-5 (Example 8) is a Akt inhibitor with IC50 values of 450 nM and 400 nM for Akt1 and Akt2, respectively .
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1
1 Cited Publications
Cat. No.: HY-13072
CAS No.: 871357-89-0
Purity:  99.86%
Synonyms: AS-703569; R-763
Research Areas:  

Cancer

Cenisertib (AS-703569) is an ATP-competitive multi-kinase inhibitor that blocks the activity of Aurora-kinase-A/B, ABL1, AKT, STAT5 and FLT3. Cenisertib induces major growth-inhibitory effects by blocking the activity of several different molecular targets in neoplastic mast cells (MC). Cenisertib inhibits tumor growth in xenograft models of pancreatic, breast, colon, ovarian, and lung tumors and leukemia .
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Cat. No.: HY-149091
CAS No.: 3046228-11-6
Purity:  99.68%
Target:  

Histone Demethylase

Research Areas:  

Cancer

KDM5B-IN-4 (compound 11ad) is a lysine demethylase 5B (KDM5B) inhibitor with an IC50 of 0.025 μM KDM5B-IN-4 increases substrate H3K4me1/2/3 level by inhibiting KDM5B in PC-3 cells. KDM5B-IN-4 downregulates PI3K/AKT. KDM5B-IN-4 reduces tumor volume in mice and shows less toxic to organs .
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Cat. No.: HY-13072R
CAS No.: 871357-89-0
Synonyms: AS-703569 (Standard); R-763 (Standard)
Research Areas:  

Cancer

Cenisertib (Standard) is the analytical standard of Cenisertib. This product is intended for research and analytical applications. Cenisertib (AS-703569) is an ATP-competitive multi-kinase inhibitor that blocks the activity of Aurora-kinase-A/B, ABL1, AKT, STAT5 and FLT3. Cenisertib induces major growth-inhibitory effects by blocking the activity of several different molecular targets in neoplastic mast cells (MC). Cenisertib inhibits tumor growth in xenograft models of pancreatic, breast, colon, ovarian, and lung tumors and leukemia .
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Cat. No.: HY-178993
CAS No.: 3093148-10-5
Target:  

PI3K Akt Apoptosis

Research Areas:  

Cancer

PI3K/AKT-IN-5 (Compound 3h) is a PI3K/AKT inhibitor. PI3K/AKT-IN-5 exhibits outstanding broad-spectrum anti-cancer activity, especially being sensitive to colorectal cancer. PI3K/AKT-IN-5 significantly reduces cell colony formation, induces G2/M phase cell cycle arrest and cell apoptosis. PI3K/AKT-IN-5 can be used for research on colorectal cancer .
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Cat. No.: HY-161280
Research Areas:  

Cancer

PROTAC FLT-3 degrader 3 is a FLT-3 PROTAC degrader. PROTAC FLT-3 degrader 3 reduces the phosphorylation levels of FLT3-ITD, AKT, STAT5 and ERK. PROTAC FLT-3 degrader 3 induces apoptosis and cell cycle arrest in leukemia cells. PROTAC FLT-3 degrader 3 can be used for the research of acute myeloid leukemia .
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Cat. No.: HY-13072B
CAS No.: 1145859-64-8
Synonyms: AS-703569 benzoate; R-763 benzoate
Research Areas:  

Cancer

Cenisertib (AS-703569) benzoate is an ATP-competitive multi-kinase inhibitor that blocks the activity of Aurora-kinase-A/B, ABL1, AKT, STAT5 and FLT3. Cenisertib benzoate induces major growth-inhibitory effects by blocking the activity of several different molecular targets in neoplastic mast cells (MC). Cenisertib benzoate inhibits tumor growth in xenograft models of pancreatic, breast, colon, ovarian, and lung tumors and leukemia .
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Cat. No.: HY-187500
Target:  

Akt PROTACs RIP kinase

Research Areas:  

Others

Akt RIMTAC-1 is a Akt RIMTAC degrader (a PROTAC-like agent) with a DC50 of 3.52 μM. Akt RIMTAC-1 forms a ternary complex with AKT and RIPK1, and recruits the VHL E3 ligase complex to mediate ubiquitination and proteasomal degradation. Akt RIMTAC-1 does not alter AKT1 mRNA levels (pink: AKT ligand-5 (HY-187501); blue: RIPK1-ligand-4 (HY-187391); black: Linker (HY-23166)) .
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Cat. No.: HY-179497
Target:  

FLT3 VEGFR Akt STAT ERK Apoptosis

Research Areas:  

Cancer

FLT3-IN-37 (Compound 6z) is a potent inhibitor of FLT3-ITD, with IC50 values of 1.5 and 3.4 nM for FLT3-ITD and TEL-VEGFR2, respectively. FLT3-IN-37 exhibits high selectivity for wild-type FLT3 (WT) and c-Kit. FLT3-IN-37 inhibits FLT3 phosphorylation and downregulates the expression of p-Akt, p-STAT5, and p-ERK. FLT3-IN-37 exerts anti-leukemia effects by blocking the cell cycle and inducing apoptosis (apoptosis). FLT3-IN-37 can be used for research on acute myeloid leukemia (AML) .
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