Panaxynol

Panaxynol
Product Name Panaxynol
CAS No.: 81203-57-8
Catalog No.: CFN93212
Molecular Formula: C17H24O
Molecular Weight: 244.4 g/mol
Purity: >=98%
Type of Compound: Miscellaneous
Physical Desc.: Oil
Targets: Bcl-2/Bax | Caspase | HIF | ERK | cAMP | MAPK | PKA
Source: The roots of Saposhnikovia divaricata.
Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
Price:
Panaxynol is the most potent antiplatelet agent in ginseng and its mechanism of action is chiefly due to the inhibition of thromboxane formation. Panaxynol has neuroprotective, and anti-proliferative effects, it induces neurite outgrowth in PC12D cells via cAMP- and MAP kinase-dependent mechanisms, and protects cortical neurons from ischemia-like injury by up-regulation of HIF-1alpha expression and inhibition of apoptotic cascade. Panaxynol has inhibitory effects on the proliferation of human pancreatic cancer cell PANC-1through inhibiting cell division and down-regulating Ki67 expression.
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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.

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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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    Biochim Biophys Acta. 1989 Mar 24;990(3):315-20.
    Antiplatelet actions of panaxynol and ginsenosides isolated from ginseng.[Pubmed: 2923911]
    The antiplatelet effect of Panaxynol isolated from the diethyl ether layer was compared with those of ginsenosides from the butanol layer of Panax ginseng.
    METHODS AND RESULTS:
    Panaxynol (0.1 mg/ml) inhibited markedly the aggregation of washed platelets induced by collagen, arachidonic acid, ADP, ionophore A23187, PAF and thrombin while ginsenosides had no significant effect on the aggregation but ginsenoside Ro (1 mg/ml) inhibited the ATP release of platelets. Less inhibitory effect of Panaxynol was observed in the aggregation of platelet-rich plasma. Thromboxane B2 formation of platelets was inhibited by Panaxynol but not by ginsenosides. The antiplatelet effect of Panaxynol was dependent on the incubation time and the aggregability of platelets inhibited by Panaxynol could not easily be recovered after washing the platelets. In human platelet-rich plasma, Panaxynol prevented secondary aggregation and completely blocked ATP release from platelets induced by epinephrine and ADP. Both Panaxynol and ginsenoside Rg2 inhibited the rise of intracellular calcium caused by collagen.
    CONCLUSIONS:
    It is concluded that Panaxynol is the most potent antiplatelet agent in ginseng and its mechanism of action is chiefly due to the inhibition of thromboxane formation.
    Chem Biol Interact. 2006 Jan 5;159(1):58-64.
    Panaxynol induces neurite outgrowth in PC12D cells via cAMP- and MAP kinase-dependent mechanisms.[Pubmed: 16219303 ]
    Panaxynol, a polyacetylene ((3R)-heptadeca-1,9-diene-4,6-diyn-3-ol; syn. falcarinol), was isolated from the lipophilic fractions of Panax notoginseng, a Chinese traditional medicinal plant.
    METHODS AND RESULTS:
    In the present study, we reported the neurotrophic effects of Panaxynol on PC12D cells and mechanism involved in neurite outgrowth of the cells. Panaxynol could morphologically promote neurite outgrowth in PC12D cells, concentration-dependently reduce cell division and up-regulate molecular marker (MAP1B) expression in PC12D cells. Panaxynol induces the elevation of intracellular cAMP in PC12D cells. The neurite outgrowth in PC12D cells induced by Panaxynol could be inhibited by the protein kinase A inhibitor RpcAMPS and by MAP kinase kinase 1/2 inhibitor U0126.
    CONCLUSIONS:
    These observations reveal that Panaxynol could induce the differentiation of PC12D cells in a process similar to but distinct from that of NGF and the Panaxynol's effects were via cAMP- and MAP kinase-dependent mechanisms.
    Chem Biol Interact. 2008 Feb 15;171(3):348-54.
    Antiproliferative effect of panaxynol on RASMCs via inhibition of ERK1/2 and CREB.[Pubmed: 18199429 ]
    Panaxynol (PNN) occurs in many foods such as carrot, celery, and several reports have shown that it has neuritogenic and neuroprotective properties.
    METHODS AND RESULTS:
    In this study, we have investigated the antiproliferative effect and the mechanism of PNN on platelet-derived growth factor (PDGF)-BB-induced proliferation of rat aortic vascular smooth muscle cells (RASMCs). PNN significantly inhibited PDGF-BB-induced proliferation and DNA synthesis of RASMCs in a concentration-dependent manner. Flow cytometry analysis showed that PNN blocked the cell cycle progression at the G(1)/S phase. Preincubation of RASMCs with 9 microM PNN resulted in a significant inhibition of PDGF-BB-induced extracellular signal-regulated kinase1/2 (ERK1/2) phosphorylation expression and PDGF-BB-induced CREB phosphorylation expression.
    CONCLUSIONS:
    The results indicated that the inhibitory effect of PNN on the PDGF-BB-induced proliferation of RASMCs might be mediated by blocking phosphorylation of ERK1/2 and that of CREB.
    Chem Biol Interact. 2010 Jan 5;183(1):165-71.
    Panaxynol protects cortical neurons from ischemia-like injury by up-regulation of HIF-1alpha expression and inhibition of apoptotic cascade.[Pubmed: 19800326 ]
    Apoptosis is one of the major characteristics of delayed neuronal degeneration in neuronal injury following cerebral ischemia. Hypoxia-induced apoptosis may be co-regulated by HIF-1alpha as well as many other factors. In recent years, numerous studies concerning Panaxynol (PNN) have been reported. However, whether PNN can show anti-hypoxia properties is still unknown.
    METHODS AND RESULTS:
    In this study, the protective effects of PNN on OGD-induced neuronal apoptosis and potential mechanisms were investigated. Pretreatment of the cells with PNN for 24h following exposure to OGD resulted in a significant elevation of cell survival determined by MTT assay, LDH assay, Hoechst staining and flow cytometric assessment. In addition to enhancing the expression of HIF-1alpha, PNN also normalized the caspase-3 expression/activation and increased the Bcl-2/Bax ratio. In our study, the increased level of HIF-1alpha with decreased cellular apoptosis suggested an important role for HIF-1alpha in hypoxic neurons.
    CONCLUSIONS:
    These results indicated that the neuroprotective effects of PNN on hypoxic neurons were at least partly due to up-regulation of HIF-1alpha and raised the possibility that PNN might reduce neurodegenerative disorders and ischemic brain diseases.
    Jiangsu Medical Journal, 2015 , 41 (1) :7-10.
    Inhibitory effects of panaxynol on proliferation of human pancreatic cancer cell PANC-1[Reference: WebLink]
    To investigate the inhibitory effects of Panaxynol(PNN)on the proliferation of human pancreatic cancer cell PANC-1.
    METHODS AND RESULTS:
    PANC-1cells were divided into three PNN groups(treated with PNN 1,9and 27╬╝mol/L)and group C(control).The proliferation of PANC-1cells,changes of cell cycle and Ki67 expression were detected by MTT,flow cytometry and Western blot,respectively. Among PNN groups,the inhibition rate and cell proportion in G1 phase were increased and Ki67 expression was reduced in PNN concentration-dependent manner(P0.01).
    CONCLUSIONS:
    PNN has inhibitory effects on the proliferation of human pancreatic cancer cell PANC-1through inhibiting cell division and down-regulating Ki67 expression.
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