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    Pomolic acid
    Information
    CAS No. 13849-91-7 Price $413 / 5mg
    Catalog No.CFN99433Purity>=98%
    Molecular Weight472.7 Type of CompoundTriterpenoids
    FormulaC30H48O4Physical DescriptionPowder
    Download Manual    COA    MSDSSimilar structuralComparison (Web)
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    Biological Activity
    Description: Pomolic acid has anti-cancer, anti-inflammatory and apoptotic activities, it can induce apoptosis in SK-OV-3 cells, which is mediated by the mitochondrial-mediated intrinsic and death receptor-induced extrinsic pathways. Pomolic acid is a potent inhibitor of the aggregation of human platelets induced by ADP and Epinephrine, exhibits IC50 values close to 60 nM and 20 nM, respectively; pomolic acid does not inhibit human platelet aggregation induced by PAF, collagen, U46619 (thromboxane analogue), TRAP or arachidonic acid; suggests that the hypotensive and platelet anti-aggregating effects of pomolic acid and its potential role in cardiovascular therapy.
    Targets: HIV | Caspase | AMPK | mTOR | NO
    In vitro:
    J Nat Prod. 1998 Sep;61(9):1090-5.
    Anti-AIDS agents. 30. Anti-HIV activity of oleanolic acid, pomolic acid, and structurally related triterpenoids.[Pubmed: 9748372]

    METHODS AND RESULTS:
    Oleanolic acid (1) was identified as an anti-HIV principle from several plants, including Rosa woodsii (leaves), Prosopis glandulosa (leaves and twigs), Phoradendron juniperinum (whole plant), Syzygium claviflorum (leaves), Hyptis capitata (whole plant), and Ternstromia gymnanthera (aerial part). It inhibited HIV-1 replication in acutely infected H9 cells with an EC50 value of 1.7 microg/mL, and inhibited H9 cell growth with an IC50 value of 21.8 microg/mL [therapeutic index (T. I.) 12.8]. Pomolic acid, isolated from R. woodsii and H. capitata, was also identified as an anti-HIV agent (EC50 1.4 microg/mL, T. I. 16.6). Although ursolic acid did show anti-HIV activity (EC50 2.0 microg/mL), it was slightly toxic (IC50 6.5 microg/mL, T. I. 3.3). A new triterpene (11) was also isolated from the CHCl3-soluble fraction of R. woodsii, though it showed no anti-HIV activity. The structure of 11 was determined to be 1beta-hydroxy-2-oxoPomolic acid by spectral examination. Based on these results, we examined the anti-HIV activity of oleanolic acid- or Pomolic acid-related triterpenes isolated from several plants. In addition, we previously demonstrated that derivatives of betulinic acid, isolated from the leaves of S. claviflorum as an anti-HIV principle, exhibited extremely potent anti-HIV activity.
    CONCLUSIONS:
    Accordingly, we prepared derivatives of oleanolic acid and evaluated their anti-HIV activity. Among the oleanolic acid derivatives, 18 demonstrated most potent anti-HIV activity, with an EC50 value of 0. 0005 microg/mL and a T. I. value of 22 400.
    Phytomedicine. 2012 Apr 15;19(6):484-7.
    Pomolic acid, triterpenoid isolated from Licania pittieri, as competitive antagonist of ADP-induced aggregation of human platelets.[Pubmed: 22402243]
    Pomolic acid (PA), triterpenoid isolated from Licania pittieri, has previously shown a potent ability to inhibit adenosine diphosphate (ADP)- and epinephrine-induced human platelet aggregation.
    METHODS AND RESULTS:
    To investigate whether Pomolic acid could be an antagonist of ADP-activated receptors of human platelets (P2Y(1) and P2Y(12)), pharmacological studies were conducted to examining its ability to modulate the platelet shape change induced by a selective P2Y(1) receptor agonist MRS2365 and also the nature of its possible interaction with ADP receptors by analyzing the characteristics of log concentration-response curves of ADP constructed in the absence and in the presence of fixed concentrations of Pomolic acid , using in vitro platelet aggregation assays. Pomolic acid did not interfere with the activation of P2Y(1) receptor by MRS2365 to induce platelet shape change and displayed a competitive antagonism of ADP-induced platelet aggregation, which most probably involves competition for a single binding site in platelets. The estimated equilibrium dissociate constant (K(b)) of Pomolic acid as ADP receptor antagonist was 15.4±0.06nM.
    CONCLUSIONS:
    Together, these findings give indirect evidence for the idea that Pomolic acid could be a potent competitive antagonist of P2Y(12) receptor, and open the possibility to consider it as new member of the non-nucleotide generation of antiplatelet drugs.
    In vivo:
    Phytomedicine. 2011 Apr 15;18(6):464-9.
    Pomolic acid of Licania pittieri elicits endothelium-dependent relaxation in rat aortic rings.[Pubmed: 21112754]
    Pomolic acid has recently shown hypotensive effect in rats. The purpose of this investigation was to determine the vascular effects of this triterpenoid and to examine its mode of action.
    METHODS AND RESULTS:
    Functional experiments in rat aortic rings precontracted with norepinephrine were performed to evaluate the vasorelaxant effect of Pomolic acid. This triterpenoid induced a vasorelaxation (IC₅₀ = 2.45 μM) in a concentration- and endothelium-dependent manner and showed no effect on contractions evoked by KCl (25 mM). Pre-treatment of aortic rings with L-NAME (100 μM), methylene blue (100 μM) or glibenclamide (10 μM), totally prevented the vasorelaxation induced by Pomolic acid, while indomethacin (10 μM) had no effect on this response. Additionally, Pomolic acid relaxation was unaffected under the muscarinic- and β-adrenergic-receptor blocked ensured for atropine and propanolol respectively (10 μM each). In contrast, the vasorelaxant effect of Pomolic acid was abolished under the purinergic-receptor blocked ensured for suramin (10 μM). Finally, apyrase (0.8 U/ml) an enzyme which hydrolyses ATP and ADP did not affect Pomolic acid relaxation.
    CONCLUSIONS:
    In summary, Pomolic acid has a potent endothelium-dependent vasorelaxant effect, possibly acting through the direct activation of endothelial purinergic receptors via NO-cGMP signaling pathway, which could be part of the mechanism underlying its hypotensive effect.
    Planta Med. 2008 Feb;74(3):215-20.
    Anti-inflammatory and apoptotic activities of pomolic acid isolated from Cecropia pachystachya.[Pubmed: 18260049]

    METHODS AND RESULTS:
    The dichloromethane extract and Pomolic acid ( 5) obtained from leaves of Cecropia pachystachya both reduced carrageenan-induced paw oedema in mice. Interestingly, while the triterpenoid inhibited the in vivo production of interleukin-1beta by 39 %, it had no effect on tumour necrosis factor-alpha production. We also demonstrated that both the dichloromethane extract and 5 inhibited the viability of human polymorphonuclear (PMN) cells in a time- and dose-dependent fashion. The PMN membrane integrity was determined with the aid of flow cytometry by means of the exclusion of propidium iodide as assay. Although the cell membrane integrity was altered, neither the extract nor 5 produced cellular necrosis. Moreover, the development of hypodiploid nuclei and DNA fragmentation in the PMN cells were both dependent on dose and time. Finally, in the annexin V-FITC binding assay, compound 5 increased the total of apoptotic cells by 42 % at 100 microM and by 71 % at 200 microM with respect to the control group.
    CONCLUSIONS:
    In conclusion, both the dichloromethane extract of ambay and isolated compound 5 inhibit the viability of PMN cells through apoptosis. Since they can regulate human neutrophil functions in this way, it is likely that these substances can also limit inflammation.
    Pomolic acid Description
    Source: The herbs of Euscaphis japonica.
    Solvent: DMSO, Pyridine, Methanol, Ethanol, etc.
    Storage: Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).

    Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.

    Need more advice on solubility, usage and handling? Please email to: service@chemfaces.com

    After receiving: The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
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    Calculate Dilution Ratios(Only for Reference)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 2.1155 mL 10.5775 mL 21.1551 mL 42.3101 mL 52.8877 mL
    5 mM 0.4231 mL 2.1155 mL 4.231 mL 8.462 mL 10.5775 mL
    10 mM 0.2116 mL 1.0578 mL 2.1155 mL 4.231 mL 5.2888 mL
    50 mM 0.0423 mL 0.2116 mL 0.4231 mL 0.8462 mL 1.0578 mL
    100 mM 0.0212 mL 0.1058 mL 0.2116 mL 0.4231 mL 0.5289 mL
    * Note: If you are in the process of experiment, it's need to make the dilution ratios of the samples. The dilution data of the sheet for your reference. Normally, it's can get a better solubility within lower of Concentrations.
    Protocol
    Kinase Assay:
    Biol Pharm Bull. 2012;35(1):105-10.
    Anticancer properties of pomolic acid-induced AMP-activated protein kinase activation in MCF7 human breast cancer cells.[Pubmed: 22223345]
    AMP-activated protein kinase (AMPK) is a sensor of cellular energy status found in all eukaryotes. Recent studies indicate that AMPK activation strongly suppresses cell proliferation in tumor cells, which requires high rates of protein synthesis and de novo fatty acid synthesis for their rapid growth. Pomolic acid (PA) has been previously described as being active in inhibiting the growth of cancer cells. In this study, we investigated Pomolic acid activated AMPK, and this activity was related to proliferation and apoptosis in MCF7 breast cancer cells. Pomolic acid inhibited cell proliferation and induced sub-G(1) arrest, elevating the mRNA levels of the apoptotic genes p53 and p21. Pomolic acid activated caspase-3, -9, and poly(ADP-ribose) polymerase, and this effect was inhibited by z-VAD-fmk. AMPK activation was increased by treating cells with Pomolic acid, inactivated by treating cells with a compound C, and co-treatment consisting of Pomolic acid and aminoimidazole carboxamide ribonucleotide (AICAR) synergistically activated AMPK. These anti-cancer potentials of Pomolic acid were accompanied by effects on de novo fatty acid synthesis as shown by the decreased expression of fatty acid synthase, and decreased acetyl-CoA carboxylase activation and incorporation of [(3)H]acetyl-CoA into fatty acids. In addition, Pomolic acid inhibited key enzymes involved in protein synthesis such as mammalian target of rapamycin (mTOR), 70 kDa ribosomal protein S6 kinase (p70S6K), and eukaryotic translation initiation factor 4E-binding protein 1 (4EBP1).
    CONCLUSIONS:
    These results suggest that Pomolic acid exerts anti-cancer properties through the modulation of AMPK pathways and its value as an anti-cancer agent in breast cancer therapy.
    Cell Research:
    Oncol Lett. 2013 Jan;5(1):386-90.
    Pomolic acid induces apoptosis in SK-OV-3 human ovarian adenocarcinoma cells through the mitochondrial-mediated intrinsic and death receptor-induced extrinsic pathways.[Pubmed: 23255955 ]
    The cytotoxic effect of Pomolic acid (PA), a pentacyclic triterpene isolated from flowers of Osmanthus fragrans var. aurantiacus Makino, was investigated in SK-OV-3 human ovarian adenocarcinoma cells.
    METHODS AND RESULTS:
    PA dose-dependently inhibited the viability of SK-OV-3 cells. PA-induced apoptosis was further characterized by detection of cell surface annexin V and sub-G1 apoptotic cell populations. The number of cells immunostained with annexin V-fluorescein isothiocyanate (FITC) increased following treatment with PA. The sub-G1 cell populations also increased in PA-treated SK-OV-3 cells. PA induced the activation of caspase-8, -9 and -3, critical mediators of apoptosis signaling. PA decreased the mitochondrial transmembrane potential (ΔΨ(m)), resulting in the activation of caspase-9. In addition, PA increased the expression of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-mediated apoptosis signaling-related death receptor 5 (DR5), mediating caspase-8-involved extrinsic pathway.
    CONCLUSIONS:
    Taken together, our results indicate that PA induces apoptosis in SK-OV-3 cells, which is mediated by the mitochondrial-mediated intrinsic and death receptor-induced extrinsic pathways.