Hot Products
Hot products from BioCrick which is a professional high-purity natural products manufacturer are well known to scientists around the world because of their high purity and stability. Each product is a chemical compound or substance produced by a living organism—that is, found in nature. In the broadest sense, natural products include any substance produced by life.Natural products remain the best sources of drugs and drug leads, and this remains true today despite the fact that many pharmaceutical companies have deemphasized natural products research in favor of HTP screening of combinatorial libraries during the past 2 decades. From 1940s to date, 131 (74.8%) out of 175 small molecule anticancer drugs are natural product-based/inspired, with 85 (48.6%) being either natural products or derived therefrom. From 1981 to date, 79 (80%) out of 99 small molecule anticancer drugs are natural product-based/inspired, with 53 (53%) being either natural products or derived therefrom. Among the 20 approved small molecule New Chemical Entities (NCEs) in 2010, a half of them are natural products.
Hot products from the professional high-purity natural products manufacturer
| Cat.No. | Product Name |
|---|---|
| BCC1312 | 5-Iodotubercidin |
| Potent adenosine kinase inhibitor (IC50 = 26 nM). Also nucleoside transporter inhibitor (IC50 values are < 25 nM, 7 μM and 15 μM for inhibition of [3H]adenosine, [3H]uridine and [3H]formycin B uptake respectively). Strongly stimulates glycogen synthesis in hepatocytes via activation of glycogen synthase. Also inhibits CK1, insulin receptor tyrosine kinase, phosphorylase kinase, PKA, CK2 and PKC (IC50 values are 0.4, 3.5, 5-10, 5-10, 10.9 and 27.7 μM respectively). Decreases hippocampal DNA methylation through adenosine kinase inhibition in vivo. | |
| BCC1317 | A 438079 hydrochloride |
| Competitive P2X7 receptor antagonist (pIC50 = 6.9 for the inhibition of Ca2+ influx in the human recombinant P2X7 cell line). Devoid of activity at other P2 receptors (IC50 >> 10 μM). Possesses antinociceptive activity in models of neuropathic pain in vivo. | |
| BCC1319 | A 83-01 |
| Potent inhibitor of TGF-β type I receptor ALK5 kinase, type I activin/nodal receptor ALK4 and type I nodal receptor ALK7 (IC50 values are 12, 45 and 7.5 nM respectively). Blocks phosphorylation of Smad2 and inhibits TGF-β-induced epithelial-to-mesenchymal transition. Only weakly inhibits ALK-1, -2, -3, -6 and MAPK activity. More potent than ItemId=54518'>SB 431542 (Cat.No. 1614). Inhibits differentiation of rat induced pluripotent stem cells (riPSCs) and increases clonal expansion efficiency. Helps maintain homogeneity and long-term in vitro self-renewal of human iPSCs. | |
| BCC1322 | A-740003 |
| Potent and selective P2X7 receptor antagonist (IC50 values are 18 and 40 nM for rat and human receptors respectively). Displays selectivity over a variety of P2X and P2Y receptors up to a concentration of 100 μM. Reduces nociception in animal models of persistent neuropathic and inflammatory pain. Also reduces neuroblastoma tumor growth in mice. | |
| BCC1324 | A-867744 |
| Positive allosteric modulator of α7 nAChRs (IC50 values are 0.98 and 1.12 μM for human and rat α7 receptor ACh-evoked currents respectively, in X. laevis oocytes). Displays no activity at 5-HT3A, α3β4 or α4β2 nAChRs. Brain penetrant. | |
| BCC1366 | AR-A014418 |
| Selective glycogen synthase kinase 3 (GSK-3) inhibitor (IC50 = 104 nM). Exhibits specificity for GSK-3 over cdk2 and cdk5 (IC50 values are > 100 μM) and over 26 other kinases. Inhibits β-amyloid-mediated neurodegeneration in hippocampal slices. | |
| BCC1397 | BAM7 |
| Bax activator (EC50 = 3.3 μM); binds at the BH3-binding site. Selective for Bax over other antiapoptotic and proapoptotic proteins. Triggers Bax oligomerization in vitro; induces Bax-mediated apoptosis in mouse embryonic fibroblasts. | |
| BCC1412 | Bazedoxifene acetate |
| Potent selective estrogen receptor modulator (SERM) (IC50 values are 26 and 99 nM for ERα and ERβ respectively). Inhibits 17β-estradiol-induced proliferation in MCF-7 cells. Co-treatment with Raloxifene completely abolishes raloxifene-induced stimulation of luminal epithelial cells and myometrium. | |
