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  3. AC-73

AC-73 

Cat. No.: HY-122214
Handling Instructions

AC-73 is a first specific, orally active inhibitor of cluster of differentiation 147 (CD147), which specifically disrupts CD147 dimerization, thereby mainly suppressing the CD147/ERK1/2/STAT3/MMP-2 pathways. AC-73 inhibits the motility and invasion of hepatocellular carcinoma cells. AC-73 is also an anti-proliferative drug and an inducer of autophagy in leukemic cells.

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AC-73 Chemical Structure

AC-73 Chemical Structure

CAS No. : 775294-71-8

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Description

AC-73 is a first specific, orally active inhibitor of cluster of differentiation 147 (CD147), which specifically disrupts CD147 dimerization, thereby mainly suppressing the CD147/ERK1/2/STAT3/MMP-2 pathways. AC-73 inhibits the motility and invasion of hepatocellular carcinoma cells[1]. AC-73 is also an anti-proliferative drug and an inducer of autophagy in leukemic cells[2].

IC50 & Target

CD147[1]

In Vitro

AC-73 (5-10 μM; 24 hours; SMMC-7721 and Huh-7 cells) treatment significantly decreases the migration ability of SMMC-7721 and Huh-7 cells in a dose-dependent manner and decreases the invasion of two HCC cells in a dose-dependent manner at 24 hours. AC-73 treatment reduces HCC metastases. There are no obvious effects on cell viability when two HCC cells are treated with AC-73 at a maximum concentration of 20 μM. The possible binding sites of AC-73 on CD147 included Glu64 and Glu73 in the N-terminal IgC2 domain, which two residues are located in the dimer interface of CD147[1].
AC-73 (5-10 μM; 24 hours; SMMC-7721 cells) treatment could significantly inhibit both MMP-2 and MMP-9 mRNA expression at the concentration of 10 μM, especially MMP-2, but no obvious effect on MMP-1, MMP-3, MMP-7, MMP-11 nor MMP-13. AC-73 could dose dependently reduce the expression of MMP-2 mRNA level and secretion of the protein level using RT-qPCR analysis and gelatin zymography experiments[1].
AC-73 (5-20 μM; 6 hours; SMMC-7721 cells) treatment dose-dependently suppresses the phosphorylation of ERK1/2 and STAT3[1].

RT-PCR[1]

Cell Line: SMMC-7721 cells
Concentration: 5 μM or 10 μM
Incubation Time: 24 hours
Result: Significantly inhibited both MMP-2 and MMP-9 mRNA expression at the concentration of 10 μM. Dose dependently reduced the expression of MMP-2 mRNA level and secretion of the protein level using RT-qPCR analysis and gelatin zymography experiments.

Western Blot Analysis[1]

Cell Line: SMMC-7721 cells
Concentration: 5 μM, 10 μM or 20 μM
Incubation Time: 6 hours
Result: The phosphorylation of ERK1/2 and STAT3 was dose-dependently suppressed.
In Vivo

AC-73 (25-50 mg/kg; for 4 weeks; Male BALB/c nu/nu mice) treatment significantly decreases the incidence of metastatic foci in nude mice. AC-73 inhibits the phosphorylation of ERK1/2 and STAT3 in a dose-dependent manner. MMP-2 is also reduced by AC-73. AC-73 could not inhibit tumor cell proliferation in vivo[1].

Animal Model: Male BALB/c nu/nu mice (4-6 weeks) with SMMC-7721 cells[1]
Dosage: 25 mg/kg, 50 mg/kg
Administration: Injected; daily; for 3 weeks
Result: Significantly decreased the incidence of metastatic foci in nude mice. Inhibited the phosphorylation of ERK1/2 and STAT3 in a dose-dependent manner. MMP-2 was also reduced.
Molecular Weight

319.40

Formula

C₂₁H₂₁NO₂

CAS No.

775294-71-8

SMILES

OC(CNCC1=CC=C(C2=CC=CC=C2)C=C1)C3=CC=CC(O)=C3

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Keywords:

AC-73AC73AC 73AutophagyInhibitorinhibitorinhibit

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