Cell lines

LNCaP cells

Preparation method

The solubility of this compound in DMSO is >17.5 mg/mL. General tips for obtaining a higher concentration: Please warm the tube at 37 ℃ for 10 minutes and/or shake it in the ultrasonic bath for a while. Stock solution can be stored below -20℃ for several months.

Reacting condition

25 and 125 μmol/L

Applications

In LNCaP cells, Anacardic acid (AA) significantly inhibited cell proliferation. Anacardic acid induced G1/S cell cycle arrest of LNCaP cells. Cells at G0 /G1 stages sharply increased after treating LNCaP cells with 125 μmol/L Anacardic acid for 24 hours. The proportion of late apoptotic cells at 24 hours following Anacardic acid incubation increased significantly. Anacardic acid down-regulated AR through supressing p300. Anacardic acid up-regulated p53 through phosphorylation of p53 on Ser15.

Animal models

BALB/c mice with diesel exhaust particle- (DEP-) induced lung inflammation

Dosage form

Oral administration, 50, 150, or 250 mg/kg, 30 days

Application

In a mice model of diesel exhaust particle- (DEP-) induced lung inflammation, pretreatment with 50, 150, or 250 mg/kg of anacardic acids (p.o.) for 30 days ameliorated antioxidant enzyme activities and decreased vascular adhesion molecule in vessels. Animals that received 50 mg/kg of anacardic acids showed decreased levels of neutrophils and tumor necrosis factor in the lungs and BALF, respectively.

Other notes

Please test the solubility of all compounds indoor, and the actual solubility may slightly differ with the theoretical value. This is caused by an experimental system error and it is normal.

IC50: Noncompetitively inhibit histone acetyltransferase (HAT) activity in prostate cancer with an IC50 value of about 5.0 M.

Anacardic acid (AA) is commonly regarded as a non-specific HAT inhibitor of p300. Meanwhile, it 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. [1]

In vitro: LNCaP, a classical metastatic prostate adenocarcinoma cell line, was adopted to study the effect of AA on cell growth, cycles and apoptosis. It was found that 125 M AA significantly inhibited LNCaP cell proliferation. In addition, the G1/S cell cycles arrest and the apoptosis of LNCaP cell was induced. Further mechanistic study suggested that AA induced cell apoptosis via suppressing p300. [1]

In vivo: Diesel exhaust particle- (DEP-) induced lung inflammation model was established to study the effect of AA on inflammation in mice. Ten days before DEP-instillation stimulation, mice were orally pretreated with 50, 150, or 250 mg/kg of AA for thirty days. All doses of AA ameliorated activities of oxidative enzymes. Moreover, 50 mg/kg of AA significantly decreased the expression level of tumor necrosis factor in lung. [2]

Clinical trial: So far, no clinical study has been conducted yet.

References:
[1] Tan J, Chen B, He L, Tang Y, Jiang Z, Yin G, Wang J, Jiang X.  Anacardic acid (6-pentadecylsalicylic acid) induces apoptosis of prostate cancer cells through inhibition of androgen receptor and activation of p53 signaling. Chin J Cancer Rea. 2012 Dec; 24(4): 275–83.
[2] Carvalho A, Annoni R, Torres L, Durao A, Shimada A, Almeida F, Hebeda C, Lopes F, Dolhnikoff F, Martins M, Silva L, Farsky S, Saldiva P, Ulrich C, Owen R, Marcourakis T, Trevisan M, Mauad T.  Anacardic acid from Cashew nuts ameliorate lung damage induced by exposure to exhaust particles in mice. Evid-Based Compl Alt. 2013 Jan. DOI: org/10.1155/2013/549879.