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> Aristolochic acid A [313-67-7]

Aristolochic acid A [313-67-7]

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Aristolochic acid A

(Synonyms: TR 1736, Aristolochic Acid I, Aristolochic Acid) Copy Product Info
Aristolochic acid A is the main component of the plant extract aristolochic acids, primarily found in the herbaceous plants Aristolochia and Asarum. It significantly inhibits the activity of activator protein 1 (AP-1) and NF-κB, and downregulates the expression of the bladder cancer-associated BLCAP gene in human cells. It is commonly used to induce nephrotoxicity models.
Aristolochic acid A
Cas No. 313-67-7
Other Forms of Aristolochic acid A:
Aristolochic acid A sodiumTN763310190-99-5
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For research use only—not for human use. No sales to individuals. Use as intended only.

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Purity:99.97%
Color:White to Yellow

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COA HNMR HPLC

Product Introduction

Aristolochic acid A AI Summary
Aristolochic acid A exhibits a diverse range of bioactivities. It has demonstrated growth inhibitory activity against a human cancer cell line in the NCI's anticancer drug screening program with a GI50 value of 883.0 nM and shows significant cytotoxicity in HEK293 cells with an EC50 value of 118340.0 nM. It also exhibits antispasmodic activity in guinea pig ileum by inhibiting electrically-induced smooth muscle contraction by 64.0% and acetylcholine-induced contraction by more than 100.0%. As an inhibitor of CDK2, it has an IC50 value greater than 20,000.0 nM, indicating low potency. The compound exhibits various inhibitory effects on enzymatic and molecular interactions, such as those related to MLL-related leukemias, tau fibril formation, Cytochrome P450 3A4, and several others. It enhances SMN2 splice variant expression, activates Nrf2, and shows inhibitory effects on ALDH1A1, uPA generation, Vif-A3F interactions, Glutaminase (GLS), Hepatitis C Virus (HCV), Pin1, TDP1, and PTHR. In addition, Aristolochic acid A exhibits anti-inflammatory activity in human neutrophils by inhibiting fMLP/CB-induced superoxide anion generation and elastase release with IC50 values greater than 10.0 ug/mL. It inhibits sodium fluorescein uptake in OATP1B3- and OATP1B1-transfected CHO cells at a concentration of 10 uM, with 107.62% and 76.91% inhibition respectively. Lastly, it shows mild antibacterial activity against Escherichia coli and Pseudomonas aeruginosa, and significant antifungal activity against Candida albicans, but lacks efficacy against several other bacterial and fungal strains..
Note: Summary generated by AI. Data source: ChEMBL
Bioactivity
Description
Aristolochic acid A is the main component of the plant extract aristolochic acids, primarily found in the herbaceous plants Aristolochia and Asarum. It significantly inhibits the activity of activator protein 1 (AP-1) and NF-κB, and downregulates the expression of the bladder cancer-associated BLCAP gene in human cells. It is commonly used to induce nephrotoxicity models.
SynonymsTR 1736, Aristolochic Acid I, Aristolochic Acid
Disease Modeling Protocol
Aristolochic Acid Nephropathy (AAN) Model
  • Modeling Mechanism：

    Aristolochic acid A (AAI) accumulates in proximal tubular epithelial cells (PTEC) via organic anion transporters (OATs); it is metabolized to produce aristolochic acid-nitrosamine ions, forming AA-DNA adducts, which can lead to gene mutations and cancer risk; it directly binds to and inhibits key enzymes in the tricarboxylic acid cycle, glycolysis, and mitochondrial respiration (IDH2, MDH2, PKM, ATP synthase, etc.), resulting in mitochondrial dysfunction and energy depletion; it activates oxidative stress, endoplasmic reticulum stress, and apoptosis pathways, accompanied by a reduction in peritubular capillaries and hypoxia, ultimately leading to renal tubular atrophy and renal interstitial fibrosis.

  • Related Products：

    Aristolochic acid A (T2801)

  • Modeling Method：

    Experimental Subject：

    Mice: 129/SvEv background (wild-type/WT, TNF PTKO, TNF DNKO); male; 8–12 weeks of age

    Dosage and Administration Route：

    ① Acute model: 5 mg/kg Aristolochic acid A, dissolved in physiological saline, intraperitoneal injection (i.p.), administered consecutively for 3 days, with tissue collection on day 4;
    ② Chronic model: 4 mg/kg Aristolochic acid A, intraperitoneal injection, every other day for 6 doses, tissue collection 5 weeks after final administration;
    ③ Intervention group (optional): 2.2 mg/kg pifithrin-α, Intraperitoneal injection, Single dose on day 1 for acute model, weekly for 3 doses in chronic model;
    Control treatment: equal-volume physiological saline administered intraperitoneally; all other procedures identical.

    Dosing Frequency and Duration Model：

    Acute model (Aristolochic acid A): Once daily for 3 consecutive days;
    Chronic model (Aristolochic acid A): Administered every other day for a total of 6 doses;
    Intervention group (pifithrin-α): Single administration in acute model (synchronised with acute model Day 1); weekly administration in chronic model, cumulative total of 3 doses;
    Control group: Administered at the same frequency as the corresponding model group

  • Validation：

    1. Functional Indicators: - Acute Model: Elevated serum blood urea nitrogen (BUN), upregulated NGAL (Lcn2) mRNA expression in renal tissue (p<0.05); - Chronic Model: Significantly elevated BUN (WT group 97±9 mg/dl vs TNF PTKO group 70±7 mg/dl, p<0.05), decreased creatinine clearance; 2. Molecular Indicators: - Inflammation and fibrosis: Upregulated expression of IL-1β, TGF-β1, Col1a1, FN1 mRNA and Col-I protein in renal tissue, significantly decreased in the TNF PTKO group (p<0.05); - Cell Cycle: Flow cytometry showed an increased proportion of PTEC cells in G2/M phase and a decreased proportion in G0/G1 phase; pifithrin-α could reverse this phenotype; - Regulatory Cell Death: Bax, Bcl2, p53, and RIP3 levels in renal tissue of the chronic model. Protein expression was upregulated (p<0.05); 3. Pathological indicators: - Acute model: PAS staining showed renal tubular necrosis, lumen dilation, and epithelial swelling (damage score of WT group was significantly higher than that of TNF PTKO group, p<0.05); - Chronic model: increased area of renal interstitial fibrosis, and significantly reduced degree of fibrosis in TNF PTKO group.

*Precautions：

*References：Wen Y,et,al. TNF- α from the Proximal Nephron Exacerbates Aristolochic Acid Nephropathy. Kidney360. 2024 Jan 1;5(1):44-56.

Chemical Properties
Molecular Weight341.27
FormulaC17H11NO7
Cas No.313-67-7
SmilesCOc1cccc2c1cc([N+]([O-])=O)c1c(cc3OCOc3c21)C(O)=O
Relative Density.1.571g/cm3
Storage & Solubility Information
StorageKeep away from direct sunlight,Store under nitrogen,Store at low temperature Powder: -20°C for 3 years | In solvent: -80°C for 1 year Shipping with blue ice/Shipping at ambient temperature.
Solubility Information
DMSO: 9.13 mg/mL (26.75 mM), Sonication is recommended.
In Vivo Formulation
10% DMSO+40% PEG300+5% Tween 80+45% Saline: 1 mg/mL (2.93 mM), Sonication is recommended.
Please add the solvents sequentially, clarifying the solution as much as possible before adding the next one. Dissolve by heating and/or sonication if necessary. Working solution is recommended to be prepared and used immediately. The formulation provided above is for reference purposes only. In vivo formulations may vary and should be modified based on specific experimental conditions.
Solution Preparation Table
DMSO
1mg5mg10mg50mg
1 mM2.9302 mL14.6512 mL29.3023 mL146.5116 mL
5 mM0.5860 mL2.9302 mL5.8605 mL29.3023 mL
10 mM0.2930 mL1.4651 mL2.9302 mL14.6512 mL
20 mM0.1465 mL0.7326 mL1.4651 mL7.3256 mL
Note : The dilution table applies only to solid products. For liquid products, please calculate the stock solution based on the stated concentration and/or density.