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Purity: ≥98%
Anacardic Acid (Hydroginkgolic acid), a natural product isolated from cashew nut shell liquid, is a potent inhibitor of p300 and p300/CBP-associated factor histone acetyltranferases, which also has antibacterial activity, antimicrobial activity, prostaglandin synthase inhibition, and tyrosinase and lipoxygenase inhibition. Anacardic acid regulates the activity and expression of several other crucial enzymes including NFκB kinase, lipoxygenase (LOX-1), xanthine oxidase, tyrosinase and ureases. Therefore, this compound exerts anti-oxidation, anti-inflammation and anti-tumor activities in vitro and in vivo.
| Targets |
Anacardic Acid (Hydroginkgolic acid) targets histone acetyltransferase p300 (IC50 = 1.6 μM) [1]
Anacardic Acid (Hydroginkgolic acid) targets histone acetyltransferases (HATs) in cardiac myocytes [2] Anacardic Acid (Hydroginkgolic acid) targets cellular components of Magnaporthe oryzae (minimum inhibitory concentration, MIC = 25 μg/mL) [3] |
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| ln Vitro |
Histone acetyltransferase anacardic acid (IC50 of ~8.5 μM and ~5 μM, respectively) inhibits the HAT activities of p300 and PCAF [1]. Hyphalite growth is inhibited by anacardic acid (300 μM). In M, anacardic acid (50 μM) causes apoptosis-like traits. oryzae; caspase has no bearing on its function. Mitochondrial potential is lost when exposed to anacardic acid (1–80 μM). Antioxidant action is demonstrated by anacardic acid (1-60 μM) in M. oryzae.
Against recombinant p300 HAT, Anacardic Acid (Hydroginkgolic acid) inhibits acetyltransferase activity in a concentration-dependent manner, with an IC50 of 1.6 μM. It does not significantly inhibit other HATs such as PCAF/GCN5 at concentrations up to 10 μM. In HeLa cells, treatment with 5–20 μM Anacardic Acid (Hydroginkgolic acid) reduces global histone H3 and H4 acetylation levels, as detected by Western blot [1] - In primary neonatal rat cardiac myocytes (NRCMs) stimulated with phenylephrine (PE), Anacardic Acid (Hydroginkgolic acid) (10–50 μM) inhibits cell hypertrophy in a dose-dependent manner: it reduces cell surface area, decreases the expression of hypertrophy markers (ANP, BNP, β-MHC) at both mRNA and protein levels (detected by RT-PCR and Western blot), and suppresses PE-induced activation of p300 HAT activity and histone H3 acetylation at the ANP promoter region (detected by ChIP assay) [2] - In Magnaporthe oryzae (rice blast fungus) mycelia and conidia, Anacardic Acid (Hydroginkgolic acid) (25–100 μg/mL) induces apoptosis-like cell death: it causes nuclear condensation (DAPI staining), DNA fragmentation (TUNEL assay), loss of mitochondrial membrane potential (JC-1 staining), and accumulation of reactive oxygen species (ROS) (DCFH-DA staining). It also inhibits fungal conidiation and appressorium formation, reducing the pathogenicity of M. oryzae on rice leaves [3] |
| ln Vivo |
Anacardic acid (5 mg/kg, ip) attenuates HAT binding to the MEF2A promoter and rescues phenylephrine-induced H3K9ac hyperacetylation in C57BL/6 mice. Anacardic Acid inhibits the transcription levels of MEF2A and cardiac development-related downstream genes, attenuates the protein overexpression of cardiac downstream genes caused by phenylephrine, reverses and attenuates cardiac hypertrophy in the hearts of mice exposed to phenylephrine, and attenuates left ventricular pressure and improve cardiac function in mice with cardiac hypertrophy [2].
In C57BL/6 mice with phenylephrine (PE)-induced cardiac hypertrophy, intraperitoneal administration of Anacardic Acid (Hydroginkgolic acid) (20 mg/kg/day) for 2 weeks attenuates cardiac hypertrophy: it reduces heart weight/body weight ratio (HW/BW) and heart weight/tibia length ratio (HW/TL), improves cardiac function (echocardiography shows increased left ventricular ejection fraction and fractional shortening), and reduces myocardial fibrosis (Masson's trichrome staining). Western blot and RT-PCR analysis of heart tissues shows decreased expression of ANP, BNP, β-MHC, and acetylated histone H3, and suppressed p300 HAT activity [2] |
| Enzyme Assay |
Recombinant p300 HAT domain protein was incubated with core histones (substrate) and [3H]-acetyl-CoA in reaction buffer. Anacardic Acid (Hydroginkgolic acid) was added at concentrations ranging from 0.1 to 50 μM, and the mixture was incubated at 30°C for 30 minutes. The reaction was terminated by adding trichloroacetic acid (TCA), and the precipitated histones were collected on glass fiber filters. The radioactivity of the filters was measured by liquid scintillation counting to quantify acetylated histone levels. The inhibition rate was calculated relative to the vehicle control, and the IC50 value was determined by nonlinear regression [1]
- HAT activity assay in cardiac myocytes: Nuclear extracts from PE-stimulated NRCMs (treated with or without Anacardic Acid (Hydroginkgolic acid)) were prepared. The reaction mixture contained nuclear extract, core histones, and [3H]-acetyl-CoA, incubated at 37°C for 1 hour. TCA precipitation and filter binding were performed as described above, and radioactivity was measured to assess HAT activity [2] |
| Cell Assay |
HeLa cell histone acetylation assay: HeLa cells were seeded in 6-well plates and treated with Anacardic Acid (Hydroginkgolic acid) (5–20 μM) for 24 hours. Cells were lysed, and nuclear proteins were extracted. Equal amounts of nuclear protein were subjected to SDS-PAGE, transferred to PVDF membranes, and probed with antibodies against acetylated histone H3 (Ac-H3), acetylated histone H4 (Ac-H4), and total H3/H4 (loading controls). Protein bands were visualized by chemiluminescence, and band intensity was quantified [1]
- Neonatal rat cardiac myocyte hypertrophy assay: NRCMs were isolated from 1–3-day-old Sprague-Dawley rats and seeded in 96-well plates. After 24 hours of culture, cells were pretreated with Anacardic Acid (Hydroginkgolic acid) (10–50 μM) for 1 hour, then stimulated with PE (10 μM) for 48 hours. Cell surface area was measured by phase-contrast microscopy (n ≥ 100 cells per group). For molecular marker analysis, total RNA and protein were extracted, and RT-PCR (for ANP, BNP, β-MHC mRNA) and Western blot (for corresponding proteins) were performed [2] - Magnaporthe oryzae cell death assay: M. oryzae conidia were suspended in liquid medium and treated with Anacardic Acid (Hydroginkgolic acid) (25–100 μg/mL) for 12–24 hours. For nuclear condensation detection, conidia/mycelia were stained with DAPI and observed by fluorescence microscopy. DNA fragmentation was detected by TUNEL assay, with fluorescence intensity quantified. Mitochondrial membrane potential was assessed by JC-1 staining (red/green fluorescence ratio), and ROS levels were measured by DCFH-DA staining (fluorescence intensity at 488 nm excitation/525 nm emission) [3] |
| Animal Protocol |
Dissolved in DMSO and co-injected with ethanol; 0, 1.25, 2.5, 5, 10 mg/kg; i.p. injection
Kunming mice C57BL/6 mice (8-week-old, male) were randomly divided into three groups: control, PE-induced hypertrophy (model), and Anacardic Acid (Hydroginkgolic acid) treatment (n = 8 per group). The model and treatment groups received subcutaneous injection of PE (5 mg/kg/day) for 2 weeks to induce cardiac hypertrophy. The treatment group was concurrently given intraperitoneal injection of Anacardic Acid (Hydroginkgolic acid) (20 mg/kg/day), dissolved in DMSO (5% final concentration) diluted with saline. The control group received subcutaneous injection of saline and intraperitoneal injection of vehicle (5% DMSO in saline). At the end of treatment, echocardiography was performed to evaluate cardiac function. Mice were euthanized, hearts were excised, weighed, and processed for histological staining (H&E, Masson's trichrome) and molecular biology analysis (Western blot, RT-PCR) [2] |
| Toxicity/Toxicokinetics |
In vitro toxicity of NRCMs: Treatment with cashew acid (hydrogenated ginkgolic acid) at concentrations up to 50 μM for 48 hours did not affect cell viability (CCK-8 assay), and the release of lactate dehydrogenase (LDH) was not significantly increased compared with the control group [2]. In vivo toxicity in mice: Intraperitoneal injection of cashew acid (hydrogenated ginkgolic acid) (20 mg/kg/day) for 2 weeks did not cause significant changes in body weight, liver function (ALT, AST levels), or kidney function (BUN, creatinine levels) compared with the control group mice. Histopathological examination of liver and kidney tissues revealed no abnormal lesions or inflammation [2]. In rice blast fungus (M. oryzae), cashew acid (hydrogenated ginkgolic acid) at concentrations above 100 μg/mL could completely inhibit hyphal growth, but no cytotoxicity to mammalian cells (HeLa, NRCMs) was observed at the same concentration [1,2,3].
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| References |
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| Additional Infomation |
Anacardic acid is a hydroxybenzoic acid, which is a product of salicylic acid with pentadecyl substitution at the 6 position. It is the main component of cashew nut shell liquid and has a wide range of biological activities. It can act as an EC 2.3.1.48 (histone acetyltransferase) inhibitor, apoptosis inducer, neuroprotective agent, EC 3.4.22.69 (SARS coronavirus main protease) inhibitor, anti-coronavirus agent, antibacterial agent, anti-inflammatory agent and plant metabolite. It is a hydroxybenzoic acid and a hydroxy monocarboxylic acid. It is functionally related to salicylic acid. Cashew acid has been reported to exist in Ozoroa insignis, Knema elegans and other organisms with relevant data. Cashew acid (hydrogenated ginkgolic acid) is a natural product isolated from cashew nut shell liquid (Anacardium occidentale). It belongs to the alkylphenol class of compounds and selectively inhibits p300 HAT by competing with acetyl-CoA for binding to the active site of p300 HAT[1].
- The anti-masturbation effect of cashew acid (hydrogenated ginkgolic acid) in cardiomyocytes is mediated by the inhibition of p300-dependent histone acetylation, thereby inhibiting the transcription of mast-related genes (ANP, BNP, β-MHC)[2]. - Cashew acid (hydrogenated ginkgolic acid) induces apoptosis-like cell death in Bacillus oryzae through ROS accumulation and mitochondrial dysfunction, and inhibits the pathogenicity of the fungus by blocking appressorium formation (a key step in plant infection)[3]. - Cashew acid (hydrogenated ginkgolic acid) exhibits a higher selectivity for p300 than other HATs (e.g., PCAF, CBP) and lower toxicity to mammalian cells at pharmacologically active concentrations[1,2]. |
| Molecular Formula |
C22H36O3
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|---|---|---|
| Molecular Weight |
348.52
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| Exact Mass |
348.266
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| CAS # |
16611-84-0
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| Related CAS # |
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| PubChem CID |
167551
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| Appearance |
White to off-white solid powder
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| Density |
1.0±0.1 g/cm3
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| Boiling Point |
474.8±33.0 °C at 760 mmHg
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| Melting Point |
90-91℃
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| Flash Point |
255.1±21.9 °C
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| Vapour Pressure |
0.0±1.2 mmHg at 25°C
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| Index of Refraction |
1.515
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| LogP |
9.96
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| Hydrogen Bond Donor Count |
2
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| Hydrogen Bond Acceptor Count |
3
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| Rotatable Bond Count |
15
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| Heavy Atom Count |
25
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| Complexity |
329
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| Defined Atom Stereocenter Count |
0
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| InChi Key |
ADFWQBGTDJIESE-UHFFFAOYSA-N
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| InChi Code |
InChI=1S/C22H36O3/c1-2-3-4-5-6-7-8-9-10-11-12-13-14-16-19-17-15-18-20(23)21(19)22(24)25/h15,17-18,23H,2-14,16H2,1H3,(H,24,25)
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| Chemical Name |
2-Hydroxy-6-pentadecyl-benzoic acid
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| Synonyms |
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| 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 |
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| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
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| Solubility (In Vivo) |
Solubility in Formulation 1: 10 mg/mL (28.69 mM) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), suspension solution; with sonication.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 100.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly. Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution. Solubility in Formulation 2: 2.5 mg/mL (7.17 mM) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), suspension solution; with ultrasonication. 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 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. View More
Solubility in Formulation 3: ≥ 2.5 mg/mL (7.17 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 2.8693 mL | 14.3464 mL | 28.6928 mL | |
| 5 mM | 0.5739 mL | 2.8693 mL | 5.7386 mL | |
| 10 mM | 0.2869 mL | 1.4346 mL | 2.8693 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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