Dasatinib Monohydrate

Catalog No.S7782 Synonyms: BMS-354825 Monohydrate

Dasatinib Monohydrate Chemical Structure

Molecular Weight(MW): 506.02

Dasatinib Monohydrate is a novel, potent and multi-targeted inhibitor that targets Abl, Src and c-Kit, with IC50 of <1 nM, 0.8 nM and 79 nM, respectively.

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Cited by 58 Publications

11 Customer Reviews

  • Nature, 2016, 534(7607):341-6.. Dasatinib Monohydrate purchased from Selleck.

    Combinational treatment of kinase inhibitors induces the similar phenotype produced by PP1. All images are lateral view with dorsal to the top and anterior to the left. The combinational treatment of Dasatinib (D) or U0126 (U) with Sunitinib (SU),PTK787 (PTK), or ZM323881 (Z) resulted in the shrinkage of dorsal aorta.

    Cell Res 2011 21, 1080-1087. Dasatinib Monohydrate purchased from Selleck.

  • Cytotoxicity by Dasatinib and Nutlin-3 used alone or in combination in B-CLL patient leukemic cells. B-CLL patient leukemic cells were exposed to serial doses of Dasatinib or Nutlin- 3 used either alone or in combination, with a fixed ratio, for 48 hours. Dose-effect plots, to determine drug efficacy, are shown for representative B-CLL samples, including 3 patients carrying 17p- (Pt. #7, Pt. #8, and Pt. #10). The decrease of cell viability, labeled "effect" on the Y-axis, was determined in assays done at least twice in duplicate.

    Clin Cancer Res 2011 17, 762-770. Dasatinib Monohydrate purchased from Selleck.

    Dasatinib interferes with the p53 transcriptional activity induced by Nutlin-3. Leukemic cell lines were exposed for 24 hours to Dasatinib (10 μM) and Nutlin-3 (10 μM), used either alone or in combination, as indicated. Levels of p53 (A), MDM2 and p21 (B) were assessed by Western blot analysis of total cell lysates. Representative examples of Western blot results are shown. Tubulin staining is shown as loading control; after densitometric analyses, p53 as well as MDM2 and p21 protein levels are expressed as folds of protein modulation, by the indicated treatments, with respect to the control untreated cultures set to 1 (hatched line). *P < 0.05 with respect to the Nutlin-3-treated cultures.

     

     

    Clin Cancer Res 2011 17, 762-770. Dasatinib Monohydrate purchased from Selleck.

  • Role of Akt in Dasatinib cytotoxicity and in DasatinibtNutlin-3 synergy. A, whole cell lysates were prepared from EHEB and BJAB cell lines treated (for 16 hours) as indicated, and hybridized with a human Phospho-Kinase array kit. Spot densities of phospho-proteins were quantified using Image Quant TL software and normalized to those of positive controls (set at 100) on the same membrane. The analysis of modulation of phosphorylation signals for P-ERK1/2, P-p38, and P-Akt are reported (*P < 0.05). Validation of phospho-kinase array results was carried out by Western blot analysis of P-Akt levels.

     

     

    Clin Cancer Res 2011 17, 762-770. Dasatinib Monohydrate purchased from Selleck.

    Impact of the TKI erlotinib, lapatinib, dasatinib, and sorafenib on the viability of MDS/AML cells. MOLM-13 (A) and HL-60 (B) cells were incubated with the indicated doses (given in mM below the x-axis) of the 4 TKI, and cellular viability was assessed by MTT assay after 24, 48 and 72 h of incubation. Changes in viability are given as percentage of cells as compared to non-treated control samples. This experiment was repeated at least three times, yielding comparable results. Graphs show representative results of one experiment carried out in duplicates (mean standard deviation).

     

     

    Biochem Pharmacol 2011 82, 1457-1466. Dasatinib Monohydrate purchased from Selleck.

  • Capacity of the TKI to overcome the AML-typical differentiation blockage. The myeloid cell lines MOLM-13 and HL-60 were incubated for 6 days with 0.01% DMSO (serving as a negative solvent control), 1 μM of ATRA (serving as a positive control), as well as with the indicated doses of the four TKI. (A) Representative May -Gruenwald -Giemsa staining of MOLM-13 cells, (B) quantitation of the percentage of MOLM-13 cells exhibiting at least two morphological signs of differentiation (that is a decrease in cytoplasmic basophilia, a reduction of the nucleo-cytoplasmic ratio, appearance of nuclear lobulation and/or cytoplasmic granules). Percentages were evaluated by examining at least 100 cells/condition; (C) representative FACS overlays of MOLM-13 cells depicting TKI-induced CD11b expression (black line) as compared to the isotype (shaded grey); (D) quantitation of TKI-induced CD11b-expression in MOLM-13 cells; (E) representative slides depicting morphology/staining of MOLM-13 cells assessed in the NBT-reduction assay; (F) respective quantitative assessment demonstrating the NBT-reducing capacity under the different drugs; (G) representative May-Gruenwald-Giemsa staining of HL-60 cells.

     

     

    Biochem Pharmacol 2011 82, 1457-1466. Dasatinib Monohydrate purchased from Selleck.

    Cytotoxicity by Dasatinib treatment in leukemic cells.Leukemic cell lines were exposed to Dasatinib (10 μM). Upon treatment, cell viability (a) was calculated as percentage with respect to the control vehicle cultures (set to 100% for each cell line) and induction of apoptosis (b) was calculated as percentage of Annexin V+/PI+ cells after 48 h of treatment.

     

     

    Invest New Drugs 2010 30, 417-422. Dasatinib Monohydrate purchased from Selleck.

  • Human phospho-kinase array analysis in response to Dasatinib treatment. Whole cell lysates were prepared from EHEB (p53wt) and BJAB (p53mut) B cell lines, either left untreated or exposed to Dasatinib for 24 h, and hybridized with a human Phospho-Kinase array kit. Spot densities of phospho-proteins were quantified using Image Quant TL software and normalized to those of positive controls on the same membrane. In a, intense decreases of signal of P-p38, PERK1/2 and P-CREB in response to Dasatinib are indicated by arrows in the membranes, and intensity of corresponding spots are reported as graphics. In b, analysis of modulation of phosphorylation of STAT family members in response to Dasatinib (spots not shown). The means±SD of three independent experiments are shown. Asterisk indicates P<0.05 against untreated.

    Invest New Drugs 2010 30, 417-422. Dasatinib Monohydrate purchased from Selleck.

    Cells were either left untreated (Unt.) or exposed to Dasatinib (Das.) for 24 h. Equal amounts of cell lysates were analyzed for ERK1/2, p38 and CREB phosphorylation by Western blot using antibodies specific for the native form of the kinases and for residues that are phosphorylated (P-) in each kinase upon activation. One of three experimentswith similar results is shown. Protein bands were quantified by densitometry and level of PERK1/2, P-p38 and P-CREB expressed as arbitrary units,were calculated for each cell line after normalization to total ERK1/2, p38 and CREB respectively

     

     

    Invest New Drugs 2010 30, 417-422. Dasatinib Monohydrate purchased from Selleck.

  • Cell vability test result. Different cell lines (A2C12, Beta D5, Gamma A3, Gamma D12, A549, CaCo2,Hep G2) were treated with different concentration of Dasatinib.

     

     

    Dr. Thomas Kruwel of Fraunhofer-Institute for Toxicology and Experimental Medicine-Dasatinib (BMS-354825) purchased from Selleck. Dasatinib Monohydrate purchased from Selleck.

Purity & Quality Control

Choose Selective Src Inhibitors

Biological Activity

Description Dasatinib Monohydrate is a novel, potent and multi-targeted inhibitor that targets Abl, Src and c-Kit, with IC50 of <1 nM, 0.8 nM and 79 nM, respectively.
Targets
Abl [1]
(Cell-free assay)
Src [1]
(Cell-free assay)
c-Kit (D816V) [2]
(Cell-free assay)
c-Kit (wt) [2]
(Cell-free assay)
0.6 nM 0.8 nM 37 nM 79 nM
In vitro

Dasatinib is more effective than imatinib in inhibiting the proliferation of Ba/F3 cells expressing wild-type Bcr-Abl and Bcr-Abl mutants, with the exception of T315I. Dasatinib has a two-log (∼325-fold) increased potency relative to imatinib. Dasatinib potently inhibits wild-type Abl kinase and all mutants except T315I over a narrow range. Dasatinib directly targets wild-type and mutant Abl kinase domains and inhibits autophosphorylation and substrate phosphorylation in a concentration-dependent manner. Dasatinib displays 325-fold greater potency compared with imatinib against cells expressing wild-type Bcr-Abl. [1] The percent of colonies of TgE bone marrow cells are decreased from 100% in untreated wells to 4.12% in Dasatinib treated wells. In the presence of Dasatinib, the difference in the percentage of colonies formed by WT and TgE bone marrow cells is statistically significant. Expression of LMP2A is able to promote B lymphocyte survival and proliferation, which can be inhibited by targeting Lyn and/or c-Abl kinases through Dasatinib. [3] Dasatinib treatment inhibits Src signaling, decreases growth, and induces cell cycle arrest and apoptosis in a subset of thyroid cancer cells. Treatment with increasing doses of Dasatinib (0.019 μM to 1.25 μM) for 3 days inhibits the growth of the C643, TPC1, BCPAP, and SW1736 cell lines by about 50% at low nanomolar concentrations, while higher concentrations are required to inhibit the growth of the K1 cell line. Treatment with 10 nM or 50 nM Dasatinib results in a 9-22% increase of cells in the G1 population among BCPAP and SW1736 and K1 cells, and a corresponding 7-18% decrease in the percentage of cells in the S phase. [4]

In vivo Dasatinib reverses splenomegaly in LMP2A/MYC double transgenic mice. Dasatinib specifically prevents colony formation by LMP2A expressing bone marrow B cells and decreased spleen size in the TgE mice. Spleen mass is significantly decreased among Dasatinib treated Tg6/λ-MYC mice when compared to the control group. Dasatinib inhibits lymphadenopathy in LMP2A/MYC double transgenic mice. Dasatinib reverses splenomegaly in Rag1KO mice engrafted with tumor cells from LMP2A/MYC double transgenic mice. Dasatinib therapy inhibits Lyn phosphorylation in B lymphocyte tumors expressing LMP2A. [3]

Protocol

Kinase Assay:

[1]

+ Expand

Kinase autophosphorylation assays:

Kinase assays using wild-type and mutant glutathione S-transferase (GST)-Abl fusion proteins (c-Abl amino acids 220-498) are done. GST-Abl fusion proteins are released from glutathione-Sepharose beads before use; the concentration of ATP is 5 μM. Immediately before use in kinase autophosphorylation and in vitro peptide substrate phosphorylation assays, GST-Abl kinase domain fusion proteins are treated with LAR tyrosine phosphatase. After 1-hour incubation at 30 °C, LAR phosphatase is inactivated by addition of sodium vanadate (1 mM). Immunoblot analysis comparing untreated GST-Abl kinase to dephosphorylated GST-Abl kinase is routinely done using phosphotyrosine-specific antibody 4G10 to confirm complete (>95%) dephosphorylation of tyrosine residues and c-Abl antibody CST 2862 to confirm equal loading of GST-Abl kinase. The Dasatinib concentration range is extended to 1,000 nM for mutant T315I. These same inhibitor concentrations are used for the in vitro peptide substrate phosphorylation assays. The three inhibitors are tested over these same concentration ranges against GST-Src kinase and GST-Lyn kinase.
Cell Research:

[1]

+ Expand
  • Cell lines: Ba/F3 cell lines
  • Concentrations: ~32 nM
  • Incubation Time: 72 hours
  • Method:

    Ba/F3 cell lines are seeded in triplicate and incubated with escalating concentrations of Dasatinib for 72 hours. Proliferation is measured using a methanethiosulfonate-based viability assay. IC50 and IC90 values are reported as the mean of three independent experiments done in quadruplicate. The inhibitor concentration ranges are 0 nM to 32 nM (Dasatinib). The Dasatinib concentration range is extended to 200 nM for mutant T315I.


    (Only for Reference)
Animal Research:

[3]

+ Expand
  • Animal Models: EμLMP2A (TgE and Tg6 strains), MYC (λ-MYC), and LMP2A/λ-MYC double transgenic mice (Tg6/λ-MYC)
  • Formulation: DMSO
  • Dosages: 30 mg/kg
  • Administration: Administered via i.p.
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 21 mg/mL warmed (41.5 mM)
Water Insoluble
Ethanol Insoluble
In vivo Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
2% DMSO+30% PEG 300+dd H2O
For best results, use promptly after mixing.
5mg/mL

* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

Chemical Information

Molecular Weight 506.02
Formula

C22H28ClN7O3S

CAS No. 863127-77-9
Storage powder
in solvent
Synonyms BMS-354825 Monohydrate

Bio Calculators

Molarity Calculator

Molarity Calculator

Calculate the mass, volume or concentration required for a solution. The Selleck molarity calculator is based on the following equation:

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

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*When preparing stock solutions, please always use the batch-specific molecular weight of the product found on the via label and MSDS / COA (available on product pages).

Dilution Calculator

Dilution Calculator

Calculate the dilution required to prepare a stock solution. The Selleck dilution calculator is based on the following equation:

Concentration (start) x Volume (start) = Concentration (final) x Volume (final)

This equation is commonly abbreviated as: C1V1 = C2V2 ( Input Output )

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* When preparing stock solutions always use the batch-specific molecular weight of the product found on the vial label and MSDS / COA (available online).

The Serial Dilution Calculator Equation

  • Serial Dilutions

  • Computed Result

  • C1=C0/X C1: LOG(C1):
    C2=C1/X C2: LOG(C2):
    C3=C2/X C3: LOG(C3):
    C4=C3/X C4: LOG(C4):
    C5=C4/X C5: LOG(C5):
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Molecular Weight Calculator

Molecular Weight Calculator

Enter the chemical formula of a compound to calculate its molar mass and elemental composition:

Total Molecular Weight: g/mol

Tip: Chemical formula is case sensitive. C10H16N2O2 c10h16n2o2

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Definitions of molecular mass, molecular weight, molar mass and molar weight:

Molecular mass (molecular weight) is the mass of one molecule of a substance and is expressed in the unified atomic mass units (u). (1 u is equal to 1/12 the mass of one atom of carbon-12)
Molar mass (molar weight) is the mass of one mole of a substance and is expressed in g/mol.

Molarity Calculator

Mass Concentration Volume Molecular Weight

Clinical Trial Information

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT01445509 Active, not recruiting Solid Tumors National Cancer Institute (NCI)|National Institutes of Health Clinical Center (CC) October 27, 2008 Phase 1
NCT03041701 Not yet recruiting Rhabdomyosarcoma|Rhabdomyosarcoma- Alveolar|Rhabdomyosarcoma-Embryonal National Cancer Institute (NCI)|National Institutes of Health Clinical Center (CC) January 24, 2017 Phase 1|Phase 2
NCT03023046 Not yet recruiting Adult Acute Lymphoblastic Leukemia|Adult Lymphoblastic Lymphoma|CD20 Positive|Philadelphia Chromosome Positive University of Washington|National Cancer Institute (NCI) February 2017 Phase 2
NCT03020030 Not yet recruiting Acute Lymphoblastic Leukemia, Pediatric Dana-Farber Cancer Institute|Baxalta US Inc. January 2017 Phase 3
NCT02744768 Not yet recruiting Acute Lymphoblastic Leukemia Gruppo Italiano Malattie EMatologiche dellAdulto December 2016 Phase 2
NCT02923986 Not yet recruiting Chronic Myelogenous Leukemia, Ph1-Positive Bio-Path Holdings, Inc. November 2016 Phase 1|Phase 2

Tech Support

Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

Handling Instructions

Tel: +1-832-582-8158 Ext:3

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Frequently Asked Questions

  • Question 1:

    What’s the difference between S1021 and S7782?

  • Answer:

    Usually, hydrate will be more stable and dissolve better than free base. But this compound (S1021) dissolves better in DMSO than hydrate one (S7782).

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID