Hot Natural Products & Bioactive Compounds
BioCrick offers high-purity natural products and bioactive compounds for scientific research. Our natural product collection includes compounds derived from plants, microorganisms and other biological sources and is widely used in pharmacological, biochemical and drug discovery research.
Natural products remain an important source of bioactive molecules and drug leads. BioCrick provides researchers with high-quality natural product compounds together with catalog numbers, product information and biological activity data.
Hot Products from BioCrick
Showing 529 - 536 of 9359 hot products
| Catalog No. | Product Name |
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| BCC2483 | GSK690693 |
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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.
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| BCC2491 | Finasteride |
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Antiandrogen that inhibits type II 5<span class='symbol'>α</span> reductase (IC<sub>50</sub> = 65 nM). Suppresses the conversion of testosterone to dihydrotestosterone. Reduces prostatic dihydrotestosterone levels and prostate size <em>in vivo</em>. Orally active.
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| BCC2492 | Imiquimod |
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Immunomodulator that displays antiviral and antitumor activity. Acts as a Toll-like receptor 7 (TLR7) agonist; stimulates proinflammatory cytokine production and activates NF-<span class='symbol'>κ</span>B.
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| BCC2493 | Ondansetron HCl |
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Selective 5-HT3 receptor antagonist (Ki = 6.16 nM). Antiemetic; prevents emesis induced by cytotoxic drugs and radiation.
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| BCC2494 | Alfuzosin HCl |
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Functionally uro-selective <span class='symbol'>α</span><sub>1</sub> adrenoceptor antagonist that does not discriminate between <span class='symbol'>α</span><sub>1</sub> subtypes. Inhibits increases in intraurethral pressure caused by phenylephrine-induced contraction by 81% with minor cardiovascular effects. Also relaxes corpus cavernosum tissue (pIC<sub>50</sub> = 7.64) <em>in vitro</em>.
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| BCC2495 | AS-605240 |
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Potent and selective inhibitor of PI 3-kinase <span class='symbol'>γ</span> (PI 3-K<span class='symbol'>γ</span>) (IC<sub>50</sub> = 8 nM). Displays 30-fold selectivity over PI 3-K<span class='symbol'>δ</span> and PI 3-K<span class='symbol'>β</span> and 7.5-fold selectivity over PI 3-K<span class='symbol'>α</span>. Suppresses the progression of joint inflammation and damage in both lymphocyte-independent and lymphocyte-dependent mouse models of rheumatoid arthritis. Orally active and ATP-competitive.
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| BCC2496 | Linezolid |
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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.
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| BCC2497 | Clopidogrel |
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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.
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