96 Well Format Sample Storage Tube With Screw Cap and Optional 2D Barcode

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Product Use Citation

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Customer Product Validation

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Product Description

Description & Advantages

    • A unique collection of 1018 FDA approved drugs for high throughput screening (HTS) and high content screening (HCS)
    • Locate new targets for old drugs
    • Bioactivity and safety confirmed by clinical trials
    • All compounds have been approved by FDA
    • Related to oncology, cardiology, anti-inflammatory, immunology, neuropsychiatry, analgesia etc
    • Structurally diverse, medicinally active, and cell permeable
    • Rich documentation with structure, IC50, and customer reviews
    • NMR and HPLC validated to ensure high purity

Product Details

Formulation: A collection of 1018 FDA approved drugs supplied as pre-dissolved DMSO solutions
Container: 96 Well Format Sample Storage Tube With Screw Cap and Optional 2D Barcode
Stability:
3 months -20°C in DMSO
6 months -80°C in DMSO
Shipping: Blue ice
Packaging: Inert gas

FDA-approved Drug Library Contents

Download the FDA-approved Drug Library - XLSX Download the FDA-approved Drug Library - SDF

Contents are for reference only and are subject to change without notice.

FDA-approved Drug Library Composition

FDA-approved Drug Library Composition

Customer Product Validation (10)

AS-605240 Review
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Rating
Source Nat Biotechnol ,2011, 29, 255-265. Vorinostat (SAHA, MK0683) purchased from Selleck
Method Immunofluorescence analysis
Cell Lines K562 cells
Concentrations 5 µM
Incubation Time 6 h
Results SAHA and other nonselective HDAC inhibitors increased steady-state acetylation of tubulin and histones manifested by the staining of acetylated microtubules and punctuate nuclear staining of acetylated histone.

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Source Nature, 2015, 520(7547), 368-72. Vemurafenib (PLX4032, RG7204) purchased from Selleck
Method Animal studies
Cell Lines A375 tumours
Concentrations 10 mg/kg
Incubation Time 4, 5 days
Results Although vemurafenib treatment decreased the volume of sensitive tumours (A375 alone)(b), Green fluorescent protein (GFP) staining confirmed increased numbers of resistant cells in regressing tumours, and EdU or BrdU staining confirmed their increased proliferation rate compared to the vehicletreated controls (c). Tumours comprising only resistant cells showed no growth difference when treated with vehicle or vemurafenib (d), indicating that the growth advantage of resistant cells in regressing tumours was not caused by direct effects of vemurafenib on cancer or stromal cells. In line with these findings, A375R cells co-implanted with other vemurafenib-sensitive melanoma cell lines (Colo800, LOX and UACC62) also showed an up toeightfold growthincreasecompared to vehicle-treated control groups (e). Local growth acceleration of resistant cells in the regressing subcutaneous tumours resulted in higher lung metastatic burden (f).

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Source Nature, 2015, 520(7547), 368-72. Vemurafenib (PLX4032, RG7204) purchased from Selleck
Method Immunofluorescence staining
Cell Lines A375/A375R tumours
Concentrations 0.1-1 uM
Incubation Time 5 days
Results This analysis highlighted FRA1 (also known FOSL1), a member of the AP1 transcription factor complex and effector of the ERK pathway27, as one of the putative upstream regulators of the TIS .FRA1 was downregulated in all drug-sensitive cells, but not in resistan cells, treated with vemurafenib, crizotinib and erlotinib (c, d).

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Source Nature, 2015, 517(7534), 391-5. PD0325901 purchased from Selleck
Method Western blot
Cell Lines Metabolic
Concentrations 10 mg/kg
Incubation Time 5 days
Results PD0325901 caused a decrease in PPARc phosphorylation at S112 and S273, confirming the established role of ERKs in regulating S112 and strongly suggesting a new role in regulating S273 (refs 22-24).

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Source Nature, 2014, 510(7504), 283-7. Trametinib (GSK1120212) purchased from Selleck
Method HE staining, IHC
Cell Lines Smyd3 mutant mice
Concentrations 1 mg/kg
Incubation Time 7 days
Results Administration of Kras and Kras;Smyd3 mutant mice with a normal dose of Trametinib blocked tumorigenesis in both strains, though phosphorylation of ERK1/2 was still lower in mice depleted of SMYD3. Notably, a low dose Trametinib regimen, which only partially inhibited pERK1/2 levels and the formation of neoplastic lesions in Kras mutant mice, was sufficient to block tumorigenesis and ERK1/2 activation in Smyd3 knockouts.

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Source Nature, 2011, 471, 235-9. Vorinostat (SAHA, MK0683) purchased from Selleck
Method MTT cell viability assay
Cell Lines T-ALL cell lines
Concentrations 0.01-100 uM
Incubation Time 72 h
Results It examined responsiveness to dexamethasone and the class I/II HDAC inhibitor vorinostat in a panel of T-ALL cell lines with wild type or mutant CREBBP alleles. This demonstrated sensitivity to vorinostat at clinically useful concentrations (IC50 below 1礛) in the majority of cell lines tested.

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Source Nature, 2011, 478(7369):349-55. Sunitinib Malate purchased from Selleck
Method Western immunoblots
Cell Lines Mouse pancreatic stem cells
Concentrations 12 uM
Incubation Time 2 days
Results Increased Ezh2 expression and β-cell BrdU incorporation were eliminated by simultaneous treatment with the receptor tyrosine kinase inhibitors Sunitinib.

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Source Nature, 2011, 478(7369):349-55. Sunitinib Malate purchased from Selleck
Method Immunofluorescent staining
Cell Lines Mouse pancreatic stem cells
Concentrations 12 uM
Incubation Time 2 days
Results Compared to vehicle-exposed controls, juvenile islets exposed to PDGF-AA had a sixfold increase of β-cell BrdU incorporation, an effect eliminated by simultaneous exposure to Sunitinib or U0126.

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Source Nature, 2010, 468, 973-977. Selumetinib (AZD6244) purchased from Selleck
Method Survival Assay
Cell Lines isogenic cell
Concentrations 0.01-10 μM
Incubation Time 72 h
Results The growth of M249 R4 and Pt55 R was sensitive to MEK inhibition in the presence of PLX4032

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Source Nature, 2010, 468, 968-972. Selumetinib (AZD6244) purchased from Selleck
Method Immunoblotting
Cell Lines A375 cells
Concentrations 1 μM
Incubation Time
Results Ectopic COT expression in A375 and SKMEL28 cells also conferred decreased sensitivity to the MEK inhibitors CI-1040 and AZD6244, suggesting that COT expression alone was sufficient to induce this phenotype. In the setting of ectopic COT expression, exposure to AZD6244 or CI-1040 in combination with PLX470 (1 μM each) reduced cell growth and pERK expression more effectively than did single-agent PLX4720, even at concentrations of 10 μM.

Product Use Citation (32)

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Tags: phosphatase inhibitor library
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