| Size | Price | |
|---|---|---|
| Other Sizes |
| Targets |
Androgen receptor, NO synthesis, MAPK-NFκB pathway[1][2]
Atraric acid targets the androgen receptor (AR), functioning as a specific, competitive antagonist. It inhibits AR-mediated transactivation without affecting the closely related glucocorticoid receptor (GR) or progesterone receptor (PR), demonstrating selectivity for AR. By inhibiting AR, atraric acid represses the expression of the endogenous prostate-specific antigen (PSA) gene in both LNCaP and C4-2 prostate cancer cells. It also inhibits PTP1B activity in a dose-dependent manner with an IC₅₀ of 51.5 μM, suggesting potential for diabetes research. |
|---|---|
| ln Vitro |
The transactivation function mediated by dihydrotestosterone-induced human AR is repressed by atrazine (10 μM; CV1 cells)[1]. The expression of the PSA gene is inhibited in both androgen-dependent and androgen-independent PCa cells by atraric acid (10 μM)[1]. In LPS-stimulated RAW264.7 cells, traric acid (1-300 μM; 24 h) dose-dependently inhibits prostaglandin E2, nitric oxide, and pro-inflammatory cytokines, but has no effect on cell viability[2]. In LPS-stimulated RAW264.7 cells, astraricic acid (100 and 300 μM; 18 h or 4 h) exhibits anti-inflammatory effects by downregulating the expression of phosphorylated IκB, extracellular signal-regulated kinases (ERK), and nuclear factor kappa B (NFκB) signaling pathway[2].
In vitro, atraric acid is a specific androgen receptor antagonist that represses the expression of the endogenous PSA gene in both LNCaP and C4-2 prostate cancer cells. It inhibits AR-mediated transactivation without affecting GR or PR. The compound also inhibits NO and cytokine synthesis, demonstrating anti-inflammatory effects. It inhibits PTP1B activity in a dose-dependent manner with an IC₅₀ of 51.5 μM. Its activity is assessed in cell-based assays measuring AR-mediated transcriptional activity using AR-responsive reporter gene constructs and PSA expression by qPCR or ELISA. |
| ln Vivo |
In LPS-induced endotoxin shock mice, traric acid (10, 30 mg/kg; ip; single dosage) decreases pathological damages and suppresses the production of pro-inflammatory cytokines[2].
Specific in vivo activity data for atraric acid are not extensively documented in the publicly available literature. As an AR antagonist with anti-inflammatory and anticancer effects, the compound has potential applications in prostate disease research. Atraric acid derivatives have been identified as new chemical lead structures for AR antagonists for the prevention or treatment of prostate diseases. Its inhibition of PTP1B also suggests potential for diabetes research. Further in vivo studies are needed to fully characterize its efficacy and safety. |
| Enzyme Assay |
In vitro enzyme/receptor binding assays for atraric acid typically involve competitive binding experiments using androgen receptor and radiolabeled or fluorescently labeled androgen as tracer. The compound's binding affinity to AR is assessed, with IC₅₀ values determined through dose-response binding experiments. Assays are conducted in buffered solutions at physiological pH with appropriate receptor preparations. Selectivity for AR over GR and PR is confirmed through parallel binding assays. Its antagonist activity is confirmed through functional assays measuring AR-mediated transcriptional inhibition using AR-responsive reporter gene constructs.
|
| Cell Assay |
Cell Viability Assay[2]
Cell Types: RAW264.7 cells Tested Concentrations: 1-300 μM Incubation Duration: 24 h Experimental Results: Did not influence the cell viability. Western Blot Analysis[2] Cell Types: RAW264 .7 cells Tested Concentrations: 100 and 300 μM Incubation Duration: 18 h or 4 h Experimental Results: Inhibited LPS-Induced expression of iNOS and COX-2 in a dose-dependent manner. Suppressed LPS-stimulated phosphorylation of the Nfκb signaling pathway. In vitro cell-based assays for atraric acid utilize AR-positive prostate cancer cell lines such as LNCaP and C4-2. Cells are treated with varying concentrations of the compound for 24-72 hours. AR-mediated transcriptional activity is evaluated using reporter gene assays with androgen response element (ARE)-luciferase constructs. PSA expression is measured by qPCR or ELISA. Cell proliferation is assessed using MTT or CCK-8 assays. Anti-inflammatory effects are assessed by measuring NO and cytokine synthesis. PTP1B inhibition is assessed using enzymatic assays. Standard cell culture conditions (37°C, 5% CO₂) with charcoal-stripped serum are employed. |
| Animal Protocol |
Animal/Disease Models: Female balb/c (Bagg ALBino) mouse (7 weeks old , 17-20 g; LPS-induced endotoxin shock)[2]
Doses: 10, 30 mg/kg Route of Administration: ip; single dosage Experimental Results: Inhibited the production of pro-inflammatory cytokines. decreased pathological damages such as vasodilation and bleeding. In vivo animal studies with atraric acid would typically involve administration of the compound to rodent models of prostate cancer or other androgen-driven conditions. Potential study designs include xenograft models using AR-positive prostate cancer cell lines. Endpoints include tumor growth measurements, assessment of AR target gene expression in tumor tissues, evaluation of inflammatory markers, and pharmacokinetic profiling. All procedures must comply with institutional animal care and use guidelines. Detailed published in vivo protocols are not currently available. |
| ADME/Pharmacokinetics |
Specific pharmacokinetic data for atraric acid are not extensively documented in the publicly available literature. The compound has a molecular weight of 196.20 g/mol and a molecular formula of C₁₀H₁₂O₄. As a small molecule with favorable physicochemical properties, it may have suitable characteristics for oral bioavailability, though detailed PK parameters have not been published. The compound is typically stored under conditions recommended for research chemicals. Further studies are needed to characterize its absorption, distribution, metabolism, and excretion profile.
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| Toxicity/Toxicokinetics |
Atraric acid is intended for research use only and is not approved for human therapeutic applications. As a natural product research chemical, comprehensive toxicological data are not extensively documented in the publicly accessible literature. Standard safety precautions should be observed when handling this compound, including the use of appropriate personal protective equipment. As with all research chemicals, comprehensive toxicological profiling would be required before any consideration for clinical development. The compound should be handled in well-ventilated areas with proper waste disposal procedures.
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| References |
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| Additional Infomation |
β-Resorcinol carboxylic acid methyl ester is a 4-hydroxybenzoic acid ester. Methyl 2,4-dihydroxy-3,6-dimethylbenzoate has been reported to exist in lichens, alpine lycophytes, and other organisms with relevant data.
Atraric acid (Methyl atrarate) (CAS#: 4707-47-5) is a specific androgen receptor antagonist with anti-inflammatory and anticancer effects. It is isolated from Pygeum africanum bark. Atraric acid represses PSA gene expression in LNCaP and C4-2 cells. It inhibits AR-mediated transactivation without affecting GR or PR. It also inhibits PTP1B with an IC₅₀ of 51.5 μM. This compound is not a drug and has not undergone clinical trials. |
| Molecular Formula |
C10H12O4
|
|---|---|
| Molecular Weight |
196.20
|
| Exact Mass |
196.073
|
| CAS # |
4707-47-5
|
| PubChem CID |
78435
|
| Appearance |
White to off-white solid powder
|
| Density |
1.3±0.1 g/cm3
|
| Boiling Point |
360.7±22.0 °C at 760 mmHg
|
| Melting Point |
141-146 °C(lit.)
|
| Flash Point |
143.9±15.8 °C
|
| Vapour Pressure |
0.0±0.8 mmHg at 25°C
|
| Index of Refraction |
1.570
|
| LogP |
2.84
|
| Hydrogen Bond Donor Count |
2
|
| Hydrogen Bond Acceptor Count |
4
|
| Rotatable Bond Count |
2
|
| Heavy Atom Count |
14
|
| Complexity |
216
|
| Defined Atom Stereocenter Count |
0
|
| SMILES |
CC1=CC(=C(C(=C1C(=O)OC)O)C)O
|
| InChi Key |
UUQHKWMIDYRWHH-UHFFFAOYSA-N
|
| InChi Code |
InChI=1S/C10H12O4/c1-5-4-7(11)6(2)9(12)8(5)10(13)14-3/h4,11-12H,1-3H3
|
| Chemical Name |
methyl 2,4-dihydroxy-3,6-dimethylbenzoate
|
| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month Note: Please store this product in a sealed and protected environment (e.g. under nitrogen), avoid exposure to moisture. |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
|
| Solubility (In Vitro) |
DMSO: 100 mg/mL (509.68 mM)
|
|---|---|
| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.5 mg/mL (12.74 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly. (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 5.0968 mL | 25.4842 mL | 50.9684 mL | |
| 5 mM | 1.0194 mL | 5.0968 mL | 10.1937 mL | |
| 10 mM | 0.5097 mL | 2.5484 mL | 5.0968 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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