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    Hecogenin
    Information
    CAS No. 467-55-0 Price $118 / 20mg
    Catalog No.CFN98586Purity>=98%
    Molecular Weight430.62Type of CompoundSteroids
    FormulaC27H42O4Physical DescriptionPowder
    Download Manual    COA    MSDSSimilar structuralComparison (Web)
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    Biological Activity
    Description: Hecogenin, a steroid saponin isolated from Agave sisalana, is a potent and highly selective inhibitor of UGT1A4 with an IC50 value of 1.5 μM. Hecogenin has anti-cancer, antiproliferative,antioxidant and anti-inflammatory effects, it can protect gastro by K⁺(ATP) channels opening and the COX-2/PG pathway. Hecogenin has inhibition of human rheumatoid arthritis synovial cell survival, the effect is associated with increased apoptosis, p38 mitogen-activated protein kinase activity and upregulation of cyclooxygenase-2.
    Targets: ERK | MMP(e.g.TIMP) | COX | ATPase | Potassium Channel | p38MAPK | NO | TRPV | TNF-α | PGE | IL Receptor | PPAR | NF-kB | JNK
    In vitro:
    Anticancer Agents Med Chem. 2014;14(8):1128-35.
    Hecogenin acetate inhibits reactive oxygen species production and induces cell cycle arrest and senescence in the A549 human lung cancer cell line.[Pubmed: 25115457]
    Cellular and molecular mechanisms related to lung cancer have been extensively studied in recent years, but the availability of effective treatments is still scarce. Hecogenin acetate, a natural saponin presenting a wide spectrum of reported pharmacological activities, has been previously evaluated for its anticancer/antiproliferative activity in some in vivo and in vitro models.
    METHODS AND RESULTS:
    Here, we investigated the effects of Hecogenin acetate in a human lung cancer cell line. A549 non-small lung cancer cells were exposed to different concentrations of Hecogenin acetate and reactive species production, ERK1/2 activation, matrix metalloproteinase expression, cell cycle arrest and cell senescence parameters were evaluated. Hecogenin acetate significantly inhibited increase in intracellular reactive species production induced by H2O2. In addition, Hecogenin acetate blocked ERK1/2 phosphorylation and inhibited the increase in MMP-2 caused by H2O2. Treatment with Hecogenin acetate induced G0/G1-phase arrest at two concentrations (75 and 100 μM, 74% and 84.3% respectively), and increased the staining of senescence-associated β -galactosidase positive cells.
    CONCLUSIONS:
    These data indicate that Hecogenin acetate is able to exert anti-cancer effects by modulating reactive species production, inducing cell cycle arrest and senescence and also modulating ERK1/2 phosphorylation and MMP-2 production.
    Int J Mol Med. 2007 Oct;20(4):451-60.
    Inhibition of human rheumatoid arthritis synovial cell survival by hecogenin and tigogenin is associated with increased apoptosis, p38 mitogen-activated protein kinase activity and upregulation of cyclooxygenase-2.[Pubmed: 17786275]
    We conducted our study to assess the antiproliferative and proapoptotic potential of Hecogenin and tigogenin, two saponins which are structurally similar to diosgenin. We particularly focused our attention on mitogen-activated protein kinase (MAPK) activation in relation to apoptosis but also with the COX-2 expression and activity. Rheumatoid arthritis (RA) synoviocytes were isolated from fresh synovial biopsies obtained from five RA patients undergoing hip arthroplasty.
    METHODS AND RESULTS:
    Measurement of cell proliferation was determined using the MTT assay. Apoptosis was evaluated by studying caspase-8, caspase-9 and caspase-3 activities but also by quantification of DNA fragmentation. Quantification of human phospho-MAPKs was realized by ELISA. COX-2 expression was demonstrated by Western blot analysis and COX-2 activity by assay of endogenous prostaglandin E2 (PGE2) production. Tigogenin was more effective than Hecogenin in inducing apoptosis in human RA fibroblast-like synoviocytes (FLS) which was caspase dependent but poly(ADP-ribose) polymerase independent and characterized by DNA fragmentation. Our results demonstrated Hecogenin- and tigogenin-induced apoptosis through activation of p38 without affecting the JNK and ERK pathways. Indeed, pretreatment with a p38 inhibitor decreased saponin-induced apoptosis with a significant decrease in DNA fragmentation. Furthermore, the rate of apoptosis induced by Hecogenin or tigogenin was associated with overexpression of COX-2 correlated with overproduction of endogenous PGE2.
    CONCLUSIONS:
    These new results provide strong evidence that a family of structurally similar plant steroids is capable of inducing apoptosis in human RA FLS with different rates and different signalling pathways. This study also confirms the discussed appearance of the downregulation or upregulation of COX-2 in cell apoptosis as a function of cell type.
    In vivo:
    Molecules. 2014 Jun 19;19(6):8303-16.
    Evidence for the involvement of spinal cord-inhibitory and cytokines-modulatory mechanisms in the anti-hyperalgesic effect of hecogenin acetate, a steroidal sapogenin-acetylated, in mice.[Pubmed: 24950436]
    Hecogenin is a steroidal sapogenin largely drawn from the plants of the genus Agave, commonly known as 'sisal', and is one of the important precursors used by the pharmaceutical industry for the synthesis of steroid hormones. Hecogenin acetate (HA) is a steroidal sapogenin-acetylated that produces antinociceptive activity. Thus, we evaluate the antihyperalgesic profile of HA in mice in inflammatory models, as well as its possible involvement with c-fos expression on spinal cord area and cytokines to produces analgesic profile.
    METHODS AND RESULTS:
    Acute pretreatment with HA (5, 10, or 20 mg/kg; i.p.) inhibited the development of mechanical hyperalgesia induced by carrageenan, TNF-α, dopamine and PGE2. Additionally, the immunofluorescence data demonstrated that acute pretreatment with HA, at all doses tested, significantly inhibited Fos-like expression in the spinal cord dorsal horn normally observed after carrageenan-inflammation. Moreover, HA did not affect the motor performance of the mice as tested in the Rota rod test. This antinociceptive profile seems to be related, at least in part, to a reduction of pro-inflammatory cytokines, as IL-1β.
    CONCLUSIONS:
    The present results suggest that HA attenuates mechanical hyperalgesia by blocking the neural transmission of pain at the spinal cord levels and by cytokines-inhibitory mechanisms.
    Hecogenin Description
    Source: The roots of Aconitum carmichaeli Debx
    Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, 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 2.3222 mL 11.6112 mL 23.2223 mL 46.4447 mL 58.0558 mL
    5 mM 0.4644 mL 2.3222 mL 4.6445 mL 9.2889 mL 11.6112 mL
    10 mM 0.2322 mL 1.1611 mL 2.3222 mL 4.6445 mL 5.8056 mL
    50 mM 0.0464 mL 0.2322 mL 0.4644 mL 0.9289 mL 1.1611 mL
    100 mM 0.0232 mL 0.1161 mL 0.2322 mL 0.4644 mL 0.5806 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:
    Drug Metab Dispos. 2006 Mar;34(3):449-56.
    Selectivity of substrate (trifluoperazine) and inhibitor (amitriptyline, androsterone, canrenoic acid, hecogenin, phenylbutazone, quinidine, quinine, and sulfinpyrazone) [Pubmed: 16381668]
    Relatively few selective substrate and inhibitor probes have been identified for human UDP-glucuronosyltransferases (UGTs). This work investigated the selectivity of trifluoperazine (TFP), as a substrate, and amitriptyline, androsterone, canrenoic acid, Hecogenin, phenylbutazone, quinidine, quinine, and sulfinpyrazone, as inhibitors, for human UGTs.
    METHODS AND RESULTS:
    Selectivity was assessed using UGTs 1A1, 1A3, 1A4, 1A6, 1A7, 1A8, 1A9, 1A10, 2B7, and 2B15 expressed in HEK293 cells. TFP was confirmed as a highly selective substrate for UGT1A4. However, TFP bound extensively to both HEK293 lysate and human liver microsomes in a concentration-dependent manner (fuinc 0.20-0.59). When corrected for nonspecific binding, Km values for TFP glucuronidation were similar for both UGT1A4 (4.1 microM) and human liver microsomes (6.1+/-1.2 microM) as the enzyme sources. Of the compounds screened as inhibitors, Hecogenin, alone, was selective; significant inhibition was observed only for UGT1A4 (IC50 1.5 microM). Using phenylbutazone and quinine as "models," inhibition kinetics were variously described by competitive and noncompetitive mechanisms. Inhibition of UGT2B7 by quinidine was also investigated further, because the effects of this compound on morphine pharmacokinetics (a known UGT2B7 substrate) have been ascribed to inhibition of P-glycoprotein. Quinidine inhibited human liver microsomal and recombinant UGT2B7, with respective Ki values of 335+/-128 microM and 186 microM.
    CONCLUSIONS:
    In conclusion, TFP and Hecogenin represent selective substrate and inhibitor probes for UGT1A4, although the extensive nonselective binding of the former should be taken into account in kinetic studies. Amitriptyline, androsterone, canrenoic acid, Hecogenin, phenylbutazone, quinidine, quinine, and sulfinpyrazone are nonselective UGT inhibitors.
    Cell Research:
    Int J Oncol. 2003 Apr;22(4):899-905.
    Different contribution of apoptosis to the antiproliferative effects of diosgenin and other plant steroids, hecogenin and tigogenin, on human 1547 osteosarcoma cells.[Pubmed: 12632085]
    Regulation of growth arrest and apoptosis are, in part, controlled by the tumor suppressor p53 after its phosphorylation which causes a determinant role in its functional activation. Moreover, PPAR regulate many functions such as proliferation and apoptosis.
    METHODS AND RESULTS:
    We compared the biological activity of diosgenin with Hecogenin and tigogenin, plant steroids structurally close to diosgenin, on proliferation rate, cell cycle distribution and apoptosis in human 1547 osteosarcoma cells. We found that all three molecules have an antiproliferative effect but gel shift analysis demonstrated that none of the plant steroids transactivated PPAR in human 1547 osteosarcoma cells whereas these molecules induced NF-kappaB binding to DNA. Although these plant steroids have a very close structure, only diosgenin caused a cell cycle arrest associated with strong apoptosis. This biological action seems correlated with a large increase of p53 protein expression.
    CONCLUSIONS:
    This fact was showed by immunofluorescence analysis which confirmed that diosgenin strongly enhanced the activation of p53 in contrast to Hecogenin and tigogenin actions.
    Animal Research:
    Eur J Pharmacol. 2012 May 15;683(1-3):260-9.
    Effects of hecogenin and its possible mechanism of action on experimental models of gastric ulcer in mice.[Pubmed: 22426163]
    This study investigates the gastroprotective effects of Hecogenin, a steroid saponin isolated from Agave sisalana, on experimental models of gastric ulcer.
    METHODS AND RESULTS:
    Male Swiss mice were used in the models of ethanol- and indometacin-induced gastric ulcer. To clarify the Hecogenin mechanism of action, the roles of nitric oxide (NO), sulfhydryls (GSH), K⁺(ATP) channels and prostaglandins were also investigated, and measurements of lipid peroxidation (TBARS assay) and nitrite levels in the stomach of Hecogenin-treated and untreated animals were performed. Furthermore, the effects of Hecogenin on myeloperoxidase (MPO) release from human neutrophils were assessed in vitro. Our results showed that Hecogenin (3.1, 7.5, 15, 30, 60 and 90 mg/kg, p.o.) acutely administered, before ethanol or indomethacin, exhibited a potent gastroprotective effect. Although the pretreatments with L-NAME, an iNOS inhibitor, and capsazepine, a TRPV1 receptor agonist, were not able to reverse the Hecogenin effect, this was reversed by glibenclamide, a K⁺(ATP) blocker, and indomethacin in the model of ethanol-induced gastric lesions. The Hecogenin pretreatment normalized GSH levels and significantly reduced lipid peroxidation and nitrite levels in the stomach, as evaluated by the ethanol-induced gastric lesion model. The drug alone increased COX-2 expression and this effect was further enhanced in the presence of ethanol. It also decreased MPO release and significantly protected the gastric mucosa.
    CONCLUSIONS:
    In conclusion, we showed that Hecogenin presents a significant gastroprotective effect that seems to be mediated by K⁺(ATP) channels opening and the COX-2/PG pathway. In addition, its antioxidant and anti-inflammatory properties may play a role in the gastroprotective drug effect.