Anacardic Acid - CAS 16611-84-0
Catalog number:
16611-84-0
Category:
Inhibitor
Not Intended for Therapeutic Use. For research use only.
Molecular Formula:
C22H36O3
Molecular Weight:
348.52
COA:
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Description:
Anacardic Acid 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.
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Purity:
>98%
Synonyms:
6-pentadecylsalicylic Acid
MSDS:
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1.Anacardic acid sensitizes prostate cancer cells to radiation therapy by regulating H2AX expression.
Yao K1, Jiang X1, He L1, Tang Y1, Yin G1, Zeng Q1, Jiang Z1, Tan J1. Int J Clin Exp Pathol. 2015 Dec 1;8(12):15926-32. eCollection 2015.
Anacardic acid (6-pentadecylsalicylic acid, AA), a natural compound isolated from the traditional medicine Amphipterygiumadstringens, has been reported as potential antitumor agents in various cancers including prostate cancer (PC). However, the effects and mechanism of AA on the radiosensitivity of prostate cancer remains unknown. The results indicated that AA exhibited strong antitumor activity in PC cell lines, either as a single agentor in combination with radiation. AA significantly induced the downregulation of H2AX and p-H2AX expression, increase of cell apoptosis and decreasing of cell invasion, which were reversed by overexpressed H2AX. These results suggest that AA sensitize prostate cancer cells to radiation therapy by repressing H2AX expression.
2.Anacardic Acid, Salicylic Acid, and Oleic Acid Differentially Alter Cellular Bioenergetic Function in Breast Cancer Cells.
Radde BN1, Alizadeh-Rad N1, Price SM1, Schultz DJ2, Klinge CM1. J Cell Biochem. 2016 Mar 17. doi: 10.1002/jcb.25544. [Epub ahead of print]
Anacardic acid is a dietary and medicinal phytochemical that inhibits breast cancer cell proliferation and uncouples oxidative phosphorylation (OXPHOS) in isolated rat liver mitochondria. Since mitochondrial-targeted anticancer therapy (mitocans) may be useful in breast cancer, we examined the effect of anacardic acid on cellular bioenergetics and OXPHOS pathway proteins in breast cancer cells modeling progression to endocrine-independence: MCF-7 estrogen receptor α (ERα)+ endocrine-sensitive; LCC9 and LY2 ERα + , endocrine-resistant, and MDA-MB-231 triple negative breast cancer (TNBC) cells. At concentrations similar to cell proliferation IC50 s, anacardic acid reduced ATP-linked oxygen consumption rate (OCR), mitochondrial reserve capacity, and coupling efficiency while increasing proton leak, reflecting mitochondrial toxicity which was greater in MCF-7 compared to endocrine-resistant and TNBC cells. These results suggest tolerance in endocrine-resistant and TNBC cells to mitochondrial stress induced by anacardic acid.
3.Combinatorial treatment with anacardic acid followed by TRAIL augments induction of apoptosis in TRAIL resistant cancer cells by the regulation of p53, MAPK and NFκβ pathways.
Harsha Raj M1, Yashaswini B1, Rössler J2, Salimath BP3. Apoptosis. 2016 May;21(5):578-93. doi: 10.1007/s10495-016-1223-8.
TRAIL, an apoptosis inducing cytokine currently in phase II clinical trial, was investigated for its capability to induce apoptosis in six different human tumor cell lines out of which three cell lines showed resistance to TRAIL induced apoptosis. To investigate whether Anacardic acid (A1) an active component of Anacardium occidentale can sensitize the resistant cell lines to TRAIL induced apoptosis, we treated the resistant cells with suboptimal concentration of A1 and showed that it is a potent enhancer of TRAIL induced apoptosis which up-regulates the expression of both DR4 and DR5 receptors, which has been observed in the cellular, protein and mRNA levels. The death receptors upregulation consequent to A1 treatment was corroborated by the activation of p53 as well as phosphorylation of p38 and JNK MAP kinases and concomitant inactivation of NFκβ and ERK signaling cascades. Also, A1 modulated the expression of key apoptotic players like Bax, Bcl-2 and CAD along with the abatement of tumor angiogenesis in vivo in EAT mouse model.
4.Retinoic acid and retinaldehyde dehydrogenase are not involved in the specific induction of the follicle-stimulating hormone β subunit by trichostatin A, a selective inhibitor of histone deacetylase.
Mijiddorj T1, Kanasaki H2, Sukhbaatar U1, Oride A1, Ishihara T1, Kyo S1. Gen Comp Endocrinol. 2015 Nov 30. pii: S0016-6480(15)30035-6. doi: 10.1016/j.ygcen.2015.11.020. [Epub ahead of print]
The selective histone deacetylase inhibitor, trichostatin A (TSA), increases follicle-stimulating hormone β subunit (FSHβ) mRNA expression but not α- and luteinizing hormone β (LHβ)-subunits in both the pituitary gonadotrophic cell line LβT2 and primary cultures of rat anterior pituitary cells. TSA increased histone acetylation in whole cell lysates in both cells. In addition, retinaldehyde dehydrogenases (RALDHs), which are retinoic acid (RA)-synthesizing enzymes, were induced by TSA in these cells. Anacardic acid, a histone acetyltransferase inhibitor that prevents histone acetylation, significantly inhibited TSA-induced FSHβ mRNA expression as well as TSA-induced RALDH2 and RALDH3 mRNA expression. Similar to the effect of TSA, gonadotropin-releasing hormone stimulated RALDH expression in LβT2 cells. RA directly applied to the pituitary cells stimulated the transcriptional activity of the FSHβ promoter. In addition, α- and LHβ-subunit promoters were also activated by RA.
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CAS 16611-84-0 Anacardic Acid

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