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 |
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BCC2475 | KU 55933 |
Potent, selective and competitive ATM kinase inhibitor (Ki = 2.2 nM, IC50 values are 13, 2500, 9300, 16600, > 100000 and > 100000 nM at ATM, DNA-PK, mTOR, PI 3-kinase, PI 4-K and ATR respectively). Decreases viability of MCF-7, A549 and HCT116 cells and decreases p21CIP1 levels in vitro. Acts as a radio- and chemosensitizer for the treatment of cancer. | |
BCC2480 | Edaravone |
A radical scavenger and antioxidant which is able to protect against the effects of ischemia, probably by inhibiting the lipoxygenase system. Protects against MPTP-induced neurotoxicity. Inhibits autophagy. | |
BCC2481 | Bicalutamide |
Orally active non-steroidal androgen receptor antagonist (IC50 = 190 nM). Displays peripheral selectivity and does not effect serum levels of LH and testosterone. Exhibits potent anticancer activity in vivo. | |
BCC2482 | GDC-0879 |
Potent and selective B-Raf inhibitor (IC50 = 0.13 nM against purified B-Raf V600E). Activity reduces phospho-ERK (pERK) levels (IC50 = 63 nM in the Malme-3M cell line). Inhibits the Raf/MEK/ERK signaling pathway in V600E B-Raf mutant cell lines. Does not activate apoptotic pathways in A375 or Colo205 cell lines. Orally bioavailable. | |
BCC2483 | GSK690693 |
ATP-competitive pan-Akt kinase inhibitor (IC50 values are 2, 13 and 9 nM of Akt1, 2 and 3 respectively). Also exhibits some inhibition for AMPK, PKA and PAK and PKC isoforms (IC50 < 100 nM). Displays antiproliferative and apoptotic effects in tumor cell lines. | |
BCC2493 | Ondansetron HCl |
Selective 5-HT3 receptor antagonist (Ki = 6.16 nM). Antiemetic; prevents emesis induced by cytotoxic drugs and radiation. | |
BCC2496 | Linezolid |
Oxazolidinone antibiotic. Inhibits bacterial protein synthesis prior to chain initiation. Displays potent antibacterial activity against a variety of multidrug-resistant gram-positive microbes in vitro and in vivo. | |
BCC2497 | Clopidogrel |
Clopidogrel is an oral, thienopyridine class antiplatelet agent.Clopidogrel is converted to its active metabolite by cytochrome P450 (CYP) enzymes. Clopidogrel (1 μM) also inhibits EGF-stimulated EGF receptor, PERK expression, and cell proliferation in RGM-1 cells (P<0.05), and causes much less inhibition of EGF-stimulated cell proliferation in EGF receptor over-expressed RGM-1 cells than in RGM-1 cells (22% vs. 32% reduction). Clopidogrel increases blood vessel number, reduces polymorphonuclear count and decreases attachment and bone loss, also decreases osteoclast number in rats submitted or not to periodontal repair. Clopidogrel decreases CXCL4, CXCL12 and PDGF content compared with saline-treated rats, without affecting CXCL5. Clopidogrel (2mg and 10mg/kg/day) significantly decreases ulcer-induced gastric epithelial cell proliferation and ulcer-stimulated expressions of EGF receptor and phosphorylated extracellular signal-regulated kinase (PERK) at the ulcer margin of rats. Clopidogrel improves endothelial function and NO bioavailability in rats with congestive heart failure. Clopidogrel-treated Congestive heart failure (CHF) rat displays enhances phosphorylation of AKT and eNOS. The clopidogrel/aspirin combination shows only additive-type effects on bleeding time prolongation induced by ear transection in the rabbit, therefore showing that combined inhibition of cyclooxygenase and ADP's effects provide a marked enhanced antithrombotic efficacy. |