Catalog No.S1343 Synonyms: BN52021
Molecular Weight(MW): 424.4
Ginkgolide B is a PAFR antagonist with IC50 of 3.6 μM.
2 Customer Reviews
Functional recovery of forelimb strength (a, c) and rotarod performance (b, d) in 8-week-old wild-type (a, b) and wild-type with SCI (c, d) mice treated with DMSO vehicle solution or GB. Asterisk represents p<0.05, SCI w/GB(10-42dpi) vs. SCI w/DMSO. Number sign represents p<0.05, SCI w/GB(1-10dpi) vs. SCI w/DMSO. Plus sign represents p<0.05, GB(10-42dpi) vs. SCI w/GB (1–10 dpi). The wild-type mice injected with GB for 42 days (n=4) demonstrated similar forelimb strength and rotarod performance as those wild-type mice injected with DMSO vehicle solution (n=4). Compared to the wild-type SCI mice injected with DMSO vehicle solution for 42 days after injury (n=10), administration of GB during the subacute and chronic phases (n=7) showed an enhanced functional recovery than that during the acute inflammatory phase (n=12) after SCI.
Mol Neurobiol, 2015, 53(5):3448-3461. Ginkgolide B purchased from Selleck.
(A) Representative western blot analysis of cleaved PARP, PCNA, activated caspase 3 and β-actin in PC3 cells received irradiation (6 Gy) followed by treatment with 100 μM GB for indicated times (post-irradiation). (B) Representative western blot analysis of cleaved PARP, PCNA, activated caspase 3 and β-actin in PC3 cells treated by 100 μM GB for 48 hours post-irradiation. (C) Caspase 3 activity in PC3 cells treated by 100 μM GB for 24 hours or 48 hours post-irradiation. Signals were normalized to the fluorescence of sham-treated controls (Ctrl). Data represents at least 3 independent experiments. *P < 0.05. (D) Cell cycle distributions in PC3 cells treated by 100 μM GB for 48 hours post-irradiation. Data represents at least 3 independent experiments.
Oncotarget, 2017, 8(8): 13846-13854. Ginkgolide B purchased from Selleck.
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Choose Selective PAFR Inhibitors
|Description||Ginkgolide B is a PAFR antagonist with IC50 of 3.6 μM.|
Ginkgolide B potently inhibits a platelet-activating factor (PAF) receptor.  Treatment of PMN with ginkgolide B (0.5 μM -12 μM) stimulates a rapid and weak production of reactive oxygen species determined by chemiluminescence. Ginkgolide B potentiates the CL response induced by fMet-Leu-Phe and zymosan.  Ginkgolide B induces cyst cell differentiation and alteres the Ras/MAPK signaling pathway.  Ginkgolide B promotes the proliferation and endothelial gene expression, and markedly enhances vascular endothelial growth factor-induced migration response and the capability to incorporate into the vascular networks in EPCs. Ginkgolide B protects EPCs from H2O2-induced cell death. Ginkgolide B induces the phosphorylation of eNOS, Akt and p38, which in turn promotes cell proliferation and function. 
|In vivo||Ginkgolide B (2 μM) significantly inhibits MDCK cyst formation dose dependently, with up to 69% reduction. Ginkgolide B also significantly inhibits cyst enlargement in the MDCK cyst model, embryonic kidney cyst model, and PKD mouse model. Preischemic application of Ginkgolide B (50 mg/kg p.o.) significantly reduces neuronal damage. 30 minutes of pretreatment with Ginkgolide B (100 mg/kg, s. c.) reduces the infarct area in the mouse model of focal ischemia. In primary cultures of hippocampal neurons and astrocytes from neonatal rats, Ginkgolide B (1 μM) protects the neurons against damage caused by glutamate. Ginkgolide B (100 μM) reduces apoptotic damage induced by staurosporine.  In pentobarbitone or ethyl carbamate-anaesthetized animals, Ginkgolide B (1 mg/kg i.v. or 10 mg/kg p.o.) inhibits bronchoconstriction, the hematocrit increase and the accompanying thrombopenia and leukopenia induced by PAF-acether (33 ng/kg–100 ng/kg). Ginkgolide B at a dose of 3 mg/kg reduces the bronchoconstriction induced by aerosolized PAF-acether. Ginkgolide B at a dose of 300 μM also inhibits the superoxide production by PAF-acether-stimulated alveolar macrophages. Ginkgolide B blocks the formation of thromboxane-triggered by PAF-acether (100 ng) injected into perfused lung.Pretreatment of parenchyma lung strips with Ginkgolide B (100 μM) partially inhibits the contraction induced by PAF-acether (0.1 μM) and suppresses the accompanying release of thromboxane.  Ginkgolide B inhibits the maturation of ischemic injury.  Ginkgolide B treatment reveals marked reduction in infarction volume, brain edema and neurological deficits. Ginkgolide B also inhibitsischemia/reperfusion (I/R) induced NF-κB, microglia activation and production of pro-inflammatory cytokines. Ginkgolide B reducesBax protein levels and increases Bcl-2 protein levels in the post-ischemic brains.  Ginkgolide B attenuates platelet aggregation and inhibits phosphatidylinositol 3 kinase (PI3K) activation and Akt phosphorylation in thrombin- and collagen-activated platelets.Ginkgolide B decreases plasma PF4 and RANTES levels in ApoE−/− mice.Ginkgolide B diminishes P-selectin, PF4, RANTES, and CD40L expression in aortic plaque in ApoE−/− mice.Moreover, ginkgolide B suppresses macrophage and vascular cell adhesion protein 1 (VCAM-1) expression in aorta lesions in ApoE−/− mice.|
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|In vitro||DMSO||85 mg/mL (200.28 mM)|
|In vivo||Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
30% propylene glycol, 5% Tween 80, 65% D5W
For best results, use promptly after mixing.
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