Products with Anti-platelet aggregation bioactivity

Cat.No. Product Name
BCN1562 6-Hydroxykaempferol-3,6,7-triglucoside
1. 6-Hydroxykaempferol 3,6,7-tri-O-glucoside and 6-hydroxykaempferol 3,6-di-O-glucoside can inhibit platelet aggregation induced by collagen, they also show weak inhibitory effects on the adenosine 5'-diphosphate (ADP)- induced platelet aggregation.
BCN1709 Sambutoxin
1. Sambutoxin, a new mycotoxin produced by toxic Fusarium isolates obtained from rotted potato tubers, it can cause toxic effects in rats, including body weight loss, feed refusal, hemorrhage in the stomach and intestines, and, finally, death when rats were fed diets supplemented with 0.05 and 0.1% sambutoxin. 2. Sambutoxin inhibits rabbit platelet aggregation, which may be party due to the decrease of ATP release. 3. Sambutoxin has in vitro cytotoxicity against various human and murine tumor cells and values of sambutoxin ranged from 46.2 to 1,425.6 ng/ml.
BCN1721 Kaempferol tetraacetate
1. Kaempferol tetraacetate exhibits significant cytotoxicity in vitro against three human cell lines HL-60, U937 and SK-MEL-1. 2. Kaempferol tetraacetate is a potent antiplatelet agent.
BCN2353 Glaucocalyxin A
Glaucocalyxin A could potentially be developed as an antiplatelet and antithrombotic agent, can inhibit platelet p-selectin secretion and integrin activation by convulxin, is a GPVI selective ligand. Glaucocalyxin A has regulation of microglia activity, can attenuate lipopolysaccharide -stimulated neuroinflammation through NF-κB and p38 MAPK signaling pathways.Glaucocalyxin A may become a potential anti-fibrotic agent in Idiopathic pulmonary fibrosis (IPF) management, it can effectively ameliorate pulmonary fibrosis through the antagonism of leukocyte infiltration and proinflammatory cytokine production.
BCN2381 3-n-Butylphthalide
Dl-3-n-Butylphthalide has antihypertensive effects, may slow the progression of hypertensive nephropathy by a variety of mechanisms.3-n-Butylphthalide is effective for improving cognitive and global functioning in patients with subcortical VCIND and exhibits good safety, this effect might be mediated by preventing the decline of the central cholinergic system.

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