16611-84-0

Usage

Uses

1. Used in Neurobiology Research:
6-Pentadecylsalicylic acid is used as a histone acetylase (HAT) inhibitor to study its effects on rat cortical neurons, providing insights into the regulation of gene expression and neuronal function.
2. Used in Cellular and Molecular Biology:
It serves as a positive control in acetylation assays in vitro, helping researchers understand the role of protein acetylation in various cellular processes.
3. Used in Agricultural Applications:
6-Pentadecylsalicylic acid is used to treat agriculture from various fruit insects, showcasing its potential as a natural pesticide.
4. Used in Enzyme Research:
The derivative of this molecule has been shown to be a potent activator of human 5-lipoxygenases (5-LOX), which are enzymes involved in the production of inflammatory mediators.
5. Used in Pharmaceutical Research:
As an inhibitor of protein SUMO modification, 6-Pentadecylsalicylic acid is used to study the role of SUMOylation in cellular processes by selectively targeting the SUMO-activating enzyme E1.
6. Used in the Development of Drug Delivery Systems:
6-Pentadecylsalicylic acid is explored for its potential in enhancing the delivery, bioavailability, and therapeutic outcomes of various drugs, particularly in the context of cancer treatment.
7. Used in the Inhibition of Specific Enzymes:
It has been reported to inhibit the activity of prostaglandin synthase, tyrosinase, and lipoxygenase, which are important for various physiological and pathological processes.
8. Used in the Study of Kinase Activity:
6-Pentadecylsalicylic acid enhances Aurora kinase A autophosphorylation and kinase activity by inducing a conformational change and enhancing ATP binding, which is crucial for understanding the regulation of cell division and other cellular processes.

Biochem/physiol Actions

Target IC50: 5 μM against HAT; 8.5 μM against PCAF; 2.2 μM inhibiting protein SUMO modification using RanGAP1-C2 as substrate

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]

IC 50

noncompetitively inhibit histone acetyltransferase (hat) activity in prostate cancer with an ic50 value of about 5.0 m.

References

1) Balasubramanyam et al. (2003), Small molecule modulators of histone acetyltransferase p300; J. Biol. Chem. 278 19134 2) Sun et al. (2006), Inhibition of histone acetyltransferase activity by anacardic acid sensitizes tumor cells to ionizing radiation; FEBS Lett. 580 4353 3) Wu et al. (2011), Anacardic acid (6-Pentadecylsalicylic acid) Inhibits Tumor Angiogenesis by Targeting Src/FAK/Rho GTPases Signaling Pathway; J. Pharmacol. Exp. Ther. 339 403 4) Omanakuttan et al. (2012), Anacardic acid Inhibits the Catalytic Activity of Matrix Metalloproteinase-2 and Matrix Metalloproteinase-9; Mol. Pharmacol. 82 614 5) Sung et al. (2008), Anacardic acid (6-nonadecyl salicylic acid), an inhibitor of histone acetyltransferase, suppresses expression of nuclear factor-kB- regulated gene products involved in cell survival, proliferation, invasion, and inflammation through inhibition of the inhibitory subunit of nuclear factor-kBα kinase, leading to potentiation of apoptosis; Blood 111 4880

InChI:InChI=1/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)

Upstream product

• 22910-60-7 6-(8-pentadecenyl)salicylic acid 
• 38449-27-3 6-pentadecylsalicylic acid methyl ester 
• 217449-10-0 ethyl 6-pentadecylsalicylate 
• 629-72-1 pentadecyl bromide 
• 28817-49-4 1,1-diethoxy-2-octadecyne 
• 6555-40-4 ethyl 2-hydroxy-6-methylbenzoate 
• 76261-14-8 (15:1)-Δ⁸-anacardic acid 
• 18654-17-6 (15:2)-Δ^8,11-anacardic acid 
• 103904-73-0 (15:3)-Δ^8,11,14-anacardic acid 
• 154714-19-9 5-hydroxy-2,2-dimethyl-4H-benzo[d][1,3]dioxin-4-one 
• 303-07-1 2,6-Dihydroxybenzoic acid 
• 103904-74-1 2-hydroxy-6-[(8Z,11Z)-8,11-pentadecadienyl]benzoic acid 
• 81625-30-1 2-(ethoxycarbonyl)-3-methoxybenzyl chloride 
• 110202-78-3 (2-ethoxycarbonyl-3-methoxybenzyl)triphenylphosphonium chloride 

Downstream Products

• 38449-27-3 6-pentadecylsalicylic acid methyl ester 
• 79688-42-9 (15 : 0)-anacardic acid O-acetate 
• 501-24-6 3-n-Pentadecylphenol 
• 65446-29-9 2-methoxy-6-pentadecyl-benzoic acid methyl ester 
• 217449-10-0 ethyl 6-pentadecylsalicylate 
• 485386-80-9 ethyl 2-methoxy-6-pentadecylbenzoate 
• 52122-74-4 3-pentadecylphenyl acetate 
• 86011-65-6 3-pentadecylphenyl benzoate 
• 440094-90-6 isopropyl-2-isopropoxy-6-pentadecylbenzoate 
• 709676-40-4 propyl 2-propoxy-6-pentadecylbenzoate 
• 1363400-78-5 1-(2-methoxypentadecylbenzyl)-3,4-dihydro-1H-benzo[e][1,4]diazepin-5(2H)-one 
• 1363400-80-9 tert-butyl 4-(2-methoxy-6-pentadecylbenzyl)-1,4-diazepane-1-carboxylate 
• 1363400-82-1 tert-butyl 8-(2-methoxy-6-pentadecylbenzyl)-8-azabicyclo[3,2,1]octan-3-ylcarbamate 
• 1363400-84-3 1-(2-methoxy-6-pentadecylbenzyl)-1H-pyrazole 

Relevant academic research and scientific papers

Phenolic Lipids Derived from Cashew Nut Shell Liquid to Treat Metabolic Diseases

Metabolic diseases are increasing at staggering rates globally. The peroxisome proliferator-activated receptors (PPARα/γ/δ) are fatty acid sensors that help mitigate imbalances between energy uptake and utilization. Herein, we report compounds derived from phenolic lipids present in cashew nut shell liquid (CNSL), an abundant waste byproduct, in an effort to create effective, accessible, and sustainable drugs. Derivatives of anacardic acid and cardanol were tested for PPAR activity in HEK293 cell co-transfection assays, primary hepatocytes, and 3T3-L1 adipocytes. In vivo studies using PPAR-expressing zebrafish embryos identified CNSL derivatives with varying tissue-specific activities. LDT409 (23) is an analogue of cardanol with partial agonist activity for PPARα and PPARγ. Pharmacokinetic profiling showed that 23 is orally bioavailable with a half-life of 4 h in mice. CNSL derivatives represent a sustainable source of selective PPAR modulators with balanced intermediate affinities (EC50 ～100 nM to 10 μM) that provide distinct and favorable gene activation profiles for the treatment of diabetes and obesity.

Synthesis and Evaluation of Ginkgolic Acid Derivatives as SUMOylation Inhibitors

SUMOylation has emerged as an important post-translational modification that has been shown to modulate protein activity associated with various signaling pathways, and consequently, it has emerged as an important therapeutic target. While several natural products have been shown to inhibit enzymes involved in the SUMOylation process, there has been little progress toward the development of more selective and potent SUMOylation inhibitors. Ginkgolic acid was one of the first natural products discovered to inhibit the SUMO E1 enzyme. Despite its use to mechanistically investigate the SUMOylation process, ginkgolic acid also modulates other pathways as well. In this Letter, preliminary structure-activity relationships for ginkgolic acid as a SUMOylation inhibitor are presented.

Structure-inspired design of a sphingolipid mimic sphingosine-1-phosphate receptor agonist from a naturally occurring sphingomyelin synthase inhibitor

Ginkgolic acid obtained as a sphingomyelin synthase inhibitor from a plant extract library inspired the concept of sphingolipid mimics. Ginkgolic acid-derived N-acyl anilines and ginkgolic acid 2-phosphate (GA2P) respectively mimic ceramide and sphingosine 1-phosphate (S1P) in structure and function. The GA2P-induced phosphorylation of ERK and internalization of S1P receptor 1 (S1P1) indicated potent agonist activity. Docking studies revealed that GA2P adopts a similar binding conformation to the bound ligand ML5, which is a strong antagonist of S1P1.

Synthesis, characterization and antimicrobial evaluation of (E)-N'-[(1-(2-methoxy-6-pentadecylbenzyl)-1H-1,2,3-triazol-4-yl]-methylene)benzohydrazide derivatives

Anacardic acid (pentadecyl salicylic acid) is a phenolic constituent present in cashew nut shell liquid (Anacardium occidentale L.) and exhibits antimicrobial properties. The present paper describes the synthesis, characterization and antimicrobial evaluation of hydrazone derivatives of anacardic acid (9a-l) linked with 1,2,3-triazole ring. All the newly synthesized compounds were determined by 1H NMR, mass and IR spectroscopy. Compounds 9d, 9e, 9h, 9i and 9j exhibited strong antifungal activity against the tested fungal strains viz., A. Niger and C. albicans.

Synthesis and antibacterial activity of anacardic acid derivatives

New anacardic acid derivatives (6a -6u) were prepared from commercially available anacardic acid and tested for Gram positive and Gram negative activities. Most compounds were found to be active compared to ampicillin.

Improved inhibition of the histone acetyltransferase PCAF by an anacardic acid derivative

Several lines of evidence indicate that histone acetyltransferases (HATs) are novel drug targets for treatment of diseases like, for example, cancer and inflammation. The natural product anacardic acid is a starting point for development of small molecule inhibitors of the histone acetyltransferase (HAT) p300/CBP associated factor (PCAF). In order to optimize the inhibitory potency, a binding model for PCAF inhibition by anacardic acid was proposed and new anacardic acid derivatives were designed. Ten new derivatives were synthesized using a novel synthetic route. One compound showed a twofold improved inhibitory potency for the PCAF HAT activity and a twofold improved inhibition of histone acetylation in HEP G2 cells.

COMPOUNDS CAPABLE OF ABSORBING ULTRAVIOLET RADIATION, COMPOSITIONS CONTAINING THEM AND PROCESSES FOR THEIR PREPARATION

The molecules capable of absorbing ultraviolet radiation from the cashew nut shell liquid changes are the object of the present invention; it is also described the compositions responsible for protecting the surfaces and chemical processes for the referred molecules production.

New application of triphosgene in a convenient synthesis of 3-aryl-1,3-benzoxazine-2,4-diones from anacardic acids

In conjunction with a search program focused on utilization of cashew (Anacardium occidentale) nut shell liquid (CNSL) as starting material for the preparation of useful compounds, a convenient synthesis of novel series of 3-aryl-1, 3-benzoxazine-2, 4-diones was prepared from anacardic acids by using of the triphosgene.

SUBSTITUTED DIHYDROPYRIMIDINES, DIHYDROPYRIMIDONES AND DIHYDROPYRIMIDINETHIONES AS CALCIUM CHANNEL BLOCKERS

The present invention is directed in part towards methods of modulating the function of calcium channels with pyrimidine-based compounds. In addition, the invention describes methods of preventing and treating calcium channel-related abnormal conditions in organisms with a compound identified by the invention. Furthermore, the invention pertains to pyrimidine-based compounds and pharmaceutical compositions comprising these compounds.

Synthesis and evaluation of a new class of nifedipine analogs with T-type calcium channel blocking activity

We have synthesized a novel series of 18 dialkyl 1,4-dihydro-4-(2′alkoxy-6′-pentadecylphenyl)-2,6-dimethyl-3,5 pyddine dicarboxylates from anacardic acid, a natural compound found in cashew nut shells, and investigated their blocking action on L- and T-type calcium channels transiently expressed in tSA-201 cells. The IC50 values for L-type calcium channel block obtained with the series ranged from 1 to ～40 μM, with higher affinities being favored by increasing the size of the alkoxy group on the 4-phenyl ring and ester substituent in the 3,5 positions. A detailed analysis of the strongest L-type channel blocker of the series (PPK-12) revealed that block was poorly reversible and mediated an apparent speeding of the time course of inactivation. Moreover, in the presence of PPK-12, the midpoint of the steady state inactivation curve was shifted by 20 mV toward more hyperpolarized potentials, resulting in an increase in blocking efficacy at more depolarized holding potentials. Surprisingly, PPK-12 blocked T- and L-type calcium channels with similar affinities. One of the weakest L-type channel inhibitors (PPK-5) exhibited a T-type channel affinity that was similar to that seen with PPK-12, resulting in a 40-fold selectivity of PPK-5 for T- over L-type channels. Thus, dialkyl 1,4-dihydro-4-(2′alkoxy-6′-pentadecylphenyl)-2,6-dimethyl-3,5 pyridine dicarboxylates may serve as excellent candidates for the development of T-type calcium-channel specific blockers.