Anthraquinone-2-carboxylic acid

Cat. No. :	HY-W031757
M.Wt:	252.22
Formula:	C15H8O4
Purity:	>98 %
Solubility:	DMSO : 25 mg/mL (ultrasonic)

Introduction of 117-78-2 :

Anthraquinone-2-carboxylic acid is an orally active anthraquinone compound and Antibacterial agent. Anthraquinone-2-carboxylic acid can be isolated from Bajitian. Anthraquinone-2-carboxylic acid inhibits the activation of DPP-IV, COX-2, NF-κB and AP-1. Anthraquinone-2-carboxylic acid blocks IAV-induced activation of the RIG-I/STAT1 pathway, alleviates IAV-mediated weight loss, and protects against lethal IAV infection. Anthraquinone-2-carboxylic acid inhibits the growth of various Staphylococcus strains. It possesses potent anti-inflammatory, immunomodulatory, analgesic and antibacterial activities^[1][2][3].\n

In Vitro:Anthraquinone-2-carboxylic acid (50 μM; 6 h) potently inhibits LPS-induced expression of iNOS, TNF-α and COX-2 mRNA in RAW264.7 macrophages^[1].
Anthraquinone-2-carboxylic acid (50 μM; 16 h) potently inhibits LPS-induced COX-2 protein expression in RAW264.7 macrophages^[1].
Anthraquinone-2-carboxylic acid (50 μM) potently inhibits PMA-induced NF-κB and AP-1 promoter activities in HEK293 cells^[1].
Anthraquinone-2-carboxylic acid (0.005-100 μM; 72 h for cytotoxicity assay) inhibits the cytopathic effect induced by four different influenza virus strains in MDCK cells, with EC₅₀ values ranging from 33.34 to 73.45 μM, and shows no cytotoxicity at concentrations up to 100 μM^[2].
Anthraquinone-2-carboxylic acid (1.23-100 μM) reduces the viral RNA copy number and infectious particle yield of H1N1 PR/8 in MDCK cells in a dose-dependent manner, with the maximum inhibitory effect observed at 100 μM^[2].
Anthraquinone-2-carboxylic acid (3.7-100 μM; 24 h) reduces the expressions of PB2, NP and NS1 proteins in A549 cells in a dose-dependent manner^[2].
Anthraquinone-2-carboxylic acid (3.7-100 μM; 24 h) dose-dependently inhibits the activation of the RIG-I/STAT1 signaling pathway in A549 cells induced by H1N1 PR/8^[2].
Anthraquinone-2-carboxylic acid (18 h) inhibits the growth of various Staphylococcus strains, with an MIC of 62.5 µg/mL against S. epidermidis ATCC 12228, 125 µg/mL against S. aureus ATCC 25923 and S. epidermidis KCTC 13171, and 250 µg/mL against MRSA1, MRSA2, and S. saprophyticus ATCC 15305^[3].
Anthraquinone-2-carboxylic acid (18 h) acts synergistically with copper oxide nanoparticles against *Staphylococcus aureus* ATCC 25923, reducing its effective MIC from 125 µg/mL to 15.6 µg/mL, with a resulting FICI of 0.375^[3]. In Vivo:Anthraquinone-2-carboxylic acid (3-30 mg/kg; p.o.; three times every 8 hours in one day) reduces HCl/EtOH-induced gastric mucosal lesions by 73% and suppresses inflammatory signaling and COX-2 expression in stomach tissue^[1].
Anthraquinone-2-carboxylic acid (3-30 mg/kg; p.o.; single dose 30 minutes prior to aspirin) reduces aspirin-induced gastric mucosal lesions by 78% and suppresses neutrophil infiltration and inflammatory signaling in stomach tissue^[1].
Anthraquinone-2-carboxylic acid (3-30 mg/kg; p.o.; daily; 7 days) significantly reduces arachidonic acid-induced ear edema in mice^[1].
Anthraquinone-2-carboxylic acid (30-60 mg/kg; p.o.; single dose 60 minutes prior to acetic acid) reduces acetic acid-induced abdominal writhes by 57% and 72%, respectively, in mice^[1].
Anthraquinone-2-carboxylic acid (10-100 mg/kg; i.g.; daily; 5 days) dose-dependently protects BALB/c mice from lethal influenza A virus infection, with the 100 mg/kg dose rescuing 60% of mice, reducing viral loads in lung tissue, and mitigating lung injury and pro-inflammatory cytokine production^[2].