Pimaric Acid
(Synonyms: 海松酸) 目录号 : GC40832海松酸是一种树脂酸，已在 A.
Cas No.:127-27-5
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >90.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Pimaric acid is a resin acid that has been found in A. cordata and various pines. It reduces mRNA expression, protein levels, and promoter activity of matrix metalloproteinase-9 (MMP-9) in TNF-α-stimulated human aortic smooth muscle cells (HASMCs) in a concentration-dependent manner when used at concentrations ranging from 5 to 20 μM. Pimaric acid (10-20 μM) reduces nuclear expression and binding of the transcription factors NF-κB and AP-1 to the MMP-9 promoter in HASMCs. Pimaric acid also reduces TNF-α-induced HASMC migration to control levels when used at a concentration of 20 μg/ml.
| Cas No. | 127-27-5 | SDF | |
| 别名 | 海松酸 | ||
| Canonical SMILES | C=C[C@@]1(C)C=C2CC[C@@]3([H])[C@@](C(O)=O)(C)CCC[C@]3(C)[C@@]2([H])CC1 | ||
| 分子式 | C20H30O2 | 分子量 | 302.5 |
| 溶解度 | DMSO : 100 mg/mL (330.63 mM; Need ultrasonic) | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 3.3058 mL | 16.5289 mL | 33.0579 mL |
| 5 mM | 0.6612 mL | 3.3058 mL | 6.6116 mL |
| 10 mM | 0.3306 mL | 1.6529 mL | 3.3058 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Anticancer effects of Pimaric Acid is mediated via endoplasmic reticulum stress, caspase-dependent apoptosis, cell cycle arrest, and inhibition of cell migration in human ovarian cancer cells
Acta Biochim Pol 2022 Mar 2;69(1):245-250.PMID:35231164DOI:10.18388/abp.2020_6011.
Pimaric Acid is a naturally occurring resin and has been found to perform many pharmacological activities including, anticancer activity. However, the role of Pimaric Acid in ovarian cancer is still not known. This investigation aimed to evaluate the anticancer effects of Pimaric Acid and its molecular mechanism in human ovarian cancer cells. MTT assay was used to examine cell viability. Cell morphology was determined through phase contrast microscopy. DAPI staining and TUNEL assay were performed for apoptotic study. Examination of cell cycle phase distribution was carried out through flow cytometry. In vitro wound healing assay was used for cell migration determination. Pimaric Acid induced cytotoxicity in human ovarian cancer cells (PA-1) in a dose-dependent manner without causing too much cytotoxicity in human ovarian epithelial cells (T1074). Cell morphology in treated cancer cells showed significant changes compared to untreated controls. Furthermore, it was observed that the cytotoxic effects of Pimaric Acid were apoptosis-mediated and caspase-dependent cascade. Western blotting analysis showed that the expression of apoptosis-associated proteins like BAX, p-53 and caspase-3 was enhanced and BCL-2 expression was diminished. The induction of cytotoxicity was mediated via endoplasmic reticulum stress through expressions of related proteins which showed a tremendous increase in p-PERK, PERK, AT-4, CHOP and IRE-1 levels after treatment. Cell cycle analysis through cytometry showed significant results as it revealed G2/M phase cell cycle arrest. Furthermore, the in vitro wound healing assay showed specific anti-migratory effects of Pimaric Acid on PA-1 cells. In conclusion it can be assumed that Pimaric Acid may act as a potential anticancer agent against ovarian carcinoma, however further investigations are required to validate this initial claim.
Molecular mechanisms underlying pimaric acid-induced modulation of voltage-gated K+ channels
J Pharmacol Sci 2017 Apr;133(4):223-231.PMID:28391996DOI:10.1016/j.jphs.2017.02.013.
Voltage-gated K+ (KV) channels, which control firing and shape of action potentials in excitable cells, are supposed to be potential therapeutic targets in many types of diseases. Pimaric Acid (PiMA) is a unique opener of large conductance Ca2+-activated K+ channel. Here, we report that PiMA modulates recombinant rodent KV channel activity. The enhancement was significant at low potentials (<0 mV) but not at more positive potentials. Application of PiMA significantly shifted the voltage-activation relationships (V1/2) of rodent KV1.1, 1.2, 1.3, 1.4, 1.6 and 2.1 channels (KV1.1-KV2.1) but KV4.3 to lower potentials and prolonged their half-decay times of the deactivation (T1/2D). The amino acid sequence which is responsible for the difference in response to PiMA was examined between KV1.1-KV2.1 and KV4.3 by site-directed mutagenesis of residues in S5 and S6 segments of Kv1.1. The point mutation of Phe332 into Tyr mimics the effects of PiMA on V1/2 and T1/2D and also abolished the further change by addition of PiMA. The results indicate that PiMA enhances voltage sensitivity of KV1.1-KV2.1 channels and suggest that the lipophilic residues including Phe332 in S5 of KV1.1-KV2.1 channels may be critical for the effects of PiMA, providing beneficial information for drug development of KV channel openers.
Pimaric Acid from Aralia cordata has an inhibitory effect on TNF-α-induced MMP-9 production and HASMC migration via down-regulated NF-κB and AP-1
Chem Biol Interact 2012 Aug 30;199(2):112-9.PMID:22705379DOI:10.1016/j.cbi.2012.06.003.
Many studies have indicated that activation of matrix metalloproteinase (MMP)-9 and smooth muscle cell (SMC) migration are involved in neointimal formation and atherosclerosis. In this study, we revealed that Pimaric Acid (PiMA) purified from Aralia cordata had an inhibitory effect on MMP-9 production and migration of human aortic smooth muscle cells (HASMCs) induced by tumor necrosis factor (TNF)-α. Down-regulated MMP-9 mRNA transcription was detected in PiMA-treated cells using RT-PCR and the luciferase-tagged MMP-9 promoter assay. Results of an electrophoretic mobility shift assay indicated that PiMA-treated HASMCs showed decreased binding activity of nuclear factor (NF)-κB and activator protein-1 transcription factors. A Western-blot analysis using nuclear extract demonstrated that PiMA reduced the levels of NF-κB p65, c-Fos, p-c-Jun, Jun-D, and p-ATF2 proteins in the nucleus. In addition, TNF-α stimulated mitogen activated protein kinase (MAPK) containing extracellular signal regulated kinase 1 and 2, p38, and c-Jun N-terminal kinase was inhibited by PiMA. Using the Transwell system, we found that PiMA inhibited TNF-α stimulated HASMC migration/invasion in a dose-dependent manner. To confirm whether MAPK mediated MMP-9 expression, we used MAPK inhibitors including U0126, SB253580, and SP600125 and found that those inhibitors reduced MMP-9 expression and HASMC migration/invasion. These results suggest that PiMA has potent anti-atherosclerotic activity with inhibitory action on MMP-9 production and cell migration in TNF-α-induced HASMCs.
1,4a,7-Trimethyl-7-vinyl-1,2,3,4,4a,4b,5,6,7,9,10,10a-dodeca-hydro-phenanthrene-1-carboxylic acid
Acta Crystallogr Sect E Struct Rep Online 2009 Apr 25;65(Pt 5):o1117.PMID:21583929DOI:10.1107/S1600536809013233.
The title compound, Pimaric Acid, C(20)H(30)O(2), was isolated from a mixture of resin acids. There are three rings in the structure. The two cyclo-hexane rings have classical chair conformations with trans-fused ring junctions. The cyclo-hexene ring appears as a semi-chair.
Isolation and characterization of isopimaric acid-degrading bacteria from a sequencing batch reactor
Appl Environ Microbiol 1996 Sep;62(9):3146-51.PMID:8795202DOI:10.1128/aem.62.9.3146-3151.1996.
We isolated two aerobic, gram-negative bacteria which grew on the diterpene resin acid isopimaric acid (IpA) as the sole carbon source and electron donor. The source of the isolates was a sequencing batch reactor treating a high-strength process stream from a paper mill. The isolates, IpA-1 and IpA-2, also grew on pimaric and dehydroabietic acids, and IpA-1 grew on abietic acid. Both strains used fatty acids, but neither strain used camphor, sitosterol, or betulin. Strain IpA-1 grew anaerobically with nitrate as an electron acceptor. Strains IpA-1 and IpA-2 had growth yields of 0.19 and 0.23 g of protein per g of IpA, respectively. During growth, both strains transformed IpA carbon to approximately equal amounts of biomass, carbon dioxide, and dissolved organic carbon. In both strains, growth on IpA induced an enzymatic system which caused cell suspensions to transform all four of the above resin acids. Cell suspensions of IpA-1 and IpA-2 removed IpA at rates of 0.56 and 0.13 mumol mg of protein-1 h-1, respectively. Cultures and cell suspensions of both strains failed to completely consume Pimaric Acid and yielded small amounts of an apparent metabolite from this acid. Cultures and cell suspensions of both strains yielded large amounts of three apparent metabolites from dehydroabietic acid. Analysis of 16S rDNA sequences indicated that the isolates are distinct members of the genus Pseudomonas sensu stricto.