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| DiscoveryProbe™ FDA-approved Drug Library
1496 FDA-approved drugs |
Sample solution is provided at 25 µL, 10mM.
Click and Customize the Panel with your own choices of compounds/size/quantities/chemical forms etc.
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| Catalog No. | Product Name | Summary | Targets | CAS Number | Smiles | |
| A3298 | Cetirizine | Antihistamine | Neuroscience|Histamine Receptor | 83881-51-0 | C1CN(CCN1CCOCC(=O)O)C(C2=CC=CC=C2)C3=CC=C(C=C3)Cl | |
| A3789 | Salmeterol xinafoate | β2-adrenergic receptor agonist | GPCR/G protein|Adrenergic Receptor | 94749-08-3 | C1=CC=C(C=C1)CCCCOCCCCCCNCC(C2=CC(=C(C=C2)O)CO)O.C1=CC=C2C(=C1)C=CC(=C2O)C(=O)O | |
| A4363 | Fluvastatin Sodium | HMG-CoA reductase inhibitor | Metabolism|HMG-CoA Reductase | 93957-55-2 | CC(C)N1C2=CC=CC=C2C(=C1C=CC(CC(CC(=O)[O-])O)O)C3=CC=C(C=C3)F.[Na+] | |
| A4370 | Moclobemide (Ro 111163) | Reversible inhibitor of MAO-A | Metabolism|MAO | 71320-77-9 | C1COCCN1CCNC(=O)C2=CC=C(C=C2)Cl | |
| A8252 | Nintedanib(BIBF 1120) | VEGFR/PDGFR/FGFR inhibitor | Tyrosine Kinase/Adaptors|PDGFR | 928326-83-4 | CN1CCN(CC1)CC(=O)N(C)C2=CC=C(C=C2)NC(=C3C4=C(C=C(C=C4)C(=O)OC)NC3=O)C5=CC=CC=C5 | |
| B1792 | Montelukast Sodium | Leukotriene receptor antagonist | GPCR/G protein|CysLT1 receptor | 151767-02-1 | CC(C)(C1=CC=CC=C1CCC(C2=CC=CC(=C2)C=CC3=NC4=C(C=CC(=C4)Cl)C=C3)SCC5(CC5)CC(=O)[O-])O.[Na+] | |
| N1674 | Piperine | MAPK inhibitor | Nature Products | 94-62-2 | C1CCN(CC1)C(=O)C=CC=CC2=CC3=C(C=C2)OCO3 | |
| N1707 | Coumarin | Precursor in chemical reaction | Nature Products | 91-64-5 | C1=CC=C2C(=C1)C=CC(=O)O2 | |
| Download the FDA-approved-drug-library - XLSX Download the FDA-approved-drug-library - SDF | ||||||
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" to show IC50| Form | Pre-dissolved DMSO solutions | Stability | -20°C: 12 months -80°C: 24 months |
| Packaging | 96 Well Format Sample Storage Tube With Screw Cap and Optional 2D Barcode. | ||
| General tips | For obtaining a higher solubility , please warm the tube at 37°C and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20°C for several months. | ||
| Shipping Condition | Evaluation sample solution : ship with blue ice All other available size: ship with RT , or blue ice upon request |
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DiscoveryProbe™ FDA-approved drug library includes 1496 FDA approved drugs for high throughput screening (HTS) and high content screening (HCS). It can be used to find new targets for old drugs. The bioactivity and safety of these drugs were confirmed by clinical trials. As they are all FDA-approved drugs, the drugs screened can be used for clinical testing directly.
1. Barrows NJ, Campos RK, Powell ST, et al. A Screen of FDA-Approved Drugs for Inhibitors of Zika Virus Infection. Cell Host Microbe. 2016 Jul 27. pii: S1931-3128(16)30303-1.
Abstract
We interrogated a FDA-approved chemicals library for their ability to block infection of human HuH-7 cells by a newly isolated ZIKV strain (ZIKV MEX_I_7). In our in vitro screening assay, more than 20 out of 774 tested compounds reduced ZIKV infection. Then these compounds were further validated for inhibition of ZIKV infection in human neural, cervical and placental stem cell lines, as well as primary human amnion cells. We found that others that had no previously known antiviral activity (e.g., daptomycin) and anti-flaviviral drugs (e.g., bortezomib and mycophenolic acid) were identified as inhibitors of ZIKV infection. There were several drugs that reduced ZIKV infection across multiple cell types, which could be tested in clinical studies of ZIKV infection and provided small molecules to study ZIKV pathogenesis.
Abstract
We interrogated a FDA-approved chemicals library for their ability to block infection of human HuH-7 cells by a newly isolated ZIKV strain (ZIKV MEX_I_7). In our in vitro screening assay, more than 20 out of 774 tested compounds reduced ZIKV infection. Then these compounds were further validated for inhibition of ZIKV infection in human neural, cervical and placental stem cell lines, as well as primary human amnion cells. We found that others that had no previously known antiviral activity (e.g., daptomycin) and anti-flaviviral drugs (e.g., bortezomib and mycophenolic acid) were identified as inhibitors of ZIKV infection. There were several drugs that reduced ZIKV infection across multiple cell types, which could be tested in clinical studies of ZIKV infection and provided small molecules to study ZIKV pathogenesis.
2. Stavrovskaya IG, Narayanan MV, Zhang W, et al. Clinically approved heterocyclics act on a mitochondrial target and reduce stroke-induced pathology. J Exp Med. 2004 Jul 19;200(2):211-22.
Abstract
Mitochondria are a major checkpoint in several pathways leading to neuronal cell death and the mitochondrial permeability transition (mPT) may be critical in stroke-related injury. In order to prove this hypothesis, 1,040 FDA-approved drugs and other bioactive compounds were tested as potential mPT inhibitors. We found that 28 structurally related drugs, including tricyclic antipsychotics and antidepressants, capable of delaying the mPT. Clinically achievable doses of promethazine inhibited mPT and were protective in both in vitro and mouse models of stroke. Also, promethazine protected primary neuronal cultures subjected to oxygen-glucose deprivation and reduced neurological impairment and infarct size in mice subjected to middle cerebral artery occlusion/reperfusion. These results provided a class of safe, tolerable drugs for stroke and neurodegeneration and also provided new tools for understanding mitochondrial roles in neuronal cell death.
Abstract
Mitochondria are a major checkpoint in several pathways leading to neuronal cell death and the mitochondrial permeability transition (mPT) may be critical in stroke-related injury. In order to prove this hypothesis, 1,040 FDA-approved drugs and other bioactive compounds were tested as potential mPT inhibitors. We found that 28 structurally related drugs, including tricyclic antipsychotics and antidepressants, capable of delaying the mPT. Clinically achievable doses of promethazine inhibited mPT and were protective in both in vitro and mouse models of stroke. Also, promethazine protected primary neuronal cultures subjected to oxygen-glucose deprivation and reduced neurological impairment and infarct size in mice subjected to middle cerebral artery occlusion/reperfusion. These results provided a class of safe, tolerable drugs for stroke and neurodegeneration and also provided new tools for understanding mitochondrial roles in neuronal cell death.
