Dasatinib

Manufactured by Bristol-Myers Squibb

Sourced in United States, United Kingdom, Switzerland

Dasatinib is a tyrosine kinase inhibitor developed by Bristol-Myers Squibb for use in the treatment of certain types of cancer. It functions by inhibiting the activity of multiple tyrosine kinases, including Bcr-Abl, Src family, c-Kit, and PDGFR. Dasatinib is approved for the treatment of Philadelphia chromosome-positive chronic myeloid leukemia and acute lymphoblastic leukemia.

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Lab products found in correlation

Nilotinib, by Novartis (8 mentions) Imatinib, by Novartis (6 mentions) Imatinib, by Bristol-Myers Squibb (3 mentions) Anti paxillin, by BD (3 mentions) Gemcitabine, by Merck Group (2 mentions) Docetaxel, by Merck Group (2 mentions) Anti fak, by Cell Signaling Technology (2 mentions) Anti psrc y416, by Cell Signaling Technology (2 mentions) Anti gm130, by BD (2 mentions) Anti ppaxillin y118, by Cell Signaling Technology (2 mentions) Anti src clone 36d10, by Cell Signaling Technology (2 mentions) Phalloidin tritc, by Thermo Fisher Scientific (2 mentions) Anti lc3b, by Cell Signaling Technology (2 mentions) Anti gapdh, by Cell Signaling Technology (2 mentions) Dasatinib, by Merck Group (2 mentions) Nilotinib, by Merck Group (2 mentions) Rnaimax, by Thermo Fisher Scientific (2 mentions) Tamoxifen, by Innovative Research (1 mentions) Imatinib mesylate, by Novartis (1 mentions) Temozolomide, by Merck Group (1 mentions)

38 protocols using dasatinib

Management of Ph+ ALL with TKIs

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Once a patient was diagnosed with Ph+ ALL (days 8 to 15 of induction therapy), imatinib mesylate (Novartis, Basel, Switzerland) was initiated at a dose of 260 to 340 mg/m 2 /d. For patients who failed the treatment [14] , were diagnosed with central nervous system leukemia (CNSL), or were imatinib resistant, a second-generation TKI, dasatinib (Bristol-Myers Squibb Company, Mount Vernon, America), was administered as a replacement at an initial dose of 50 mg/m 2 /d, if the patient had no dasatinib-resistant BCR-ABL mutations, such as T315I, V299L, T315A, and F317L/V/I/C.
TKIs were continuously administered during induction, consolidation, and maintenance treatment for patients in the nontransplant cohort and were administered until initiation of the conditioning regimen of transplantation for patients in the transplant cohort. TKI administration after transplantation has been reported in previous literature [12, 15, 16] . TKIs were continuously administered for at least 12 months after HSCT. If grades III to IV myelosuppression or grades III to IV nonhematologic adverse reactions occurred during the use of TKIs, TKIs were suspended or the dose was reduced as necessary and then resumed on recovery.

Xue Y.J., Cheng Y.F., Lu A.D., Wang Y., Zuo Y.X., Yan C.H., Wu J., Sun Y.Q., Suo P., Chen Y.H., Chen H., Jia Y.P., Liu K.Y., Han W., Xu L.P., Zhang L.P, & Huang X.J. (2019). Allogeneic Hematopoietic Stem Cell Transplantation, Especially Haploidentical, May Improve Long-Term Survival for High-Risk Pediatric Patients with Philadelphia Chromosome-Positive Acute Lymphoblastic Leukemia in the Tyrosine Kinase Inhibitor Era. Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation, 25(8).

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Evaluating Tumor Growth and Metastasis

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Mouse experiments were performed as previously described [26 (link)]. Endocrine sensitive (MCF-7) and endocrine resistant (LY2) xenograft models were established. Mice were supplemented with estrogen (0.25 mg/pellet, 60-day release) and treated with tamoxifen (5 mg/pellet, 60-day release; Innovative Research of America, Sarasota, FL, USA) and dasatinib (50 mg/kg/day, oral gavage; Bristol-Myers Squibb, New York, NY, USA) as indicated. Tumor growth was recorded twice weekly by caliper measurements, and tumors were imaged using an IVIS whole body imaging system (Xenogen Corp, Alameda, CA, USA) to detect luciferase activity of the LY2-luc cells. Metastasis was detected by shielding the primary tumor, and quantitative measurements of metastatic deposits were calculated using Living Image analysis software (Xenogen). Formation of metastasis to the organs was also confirmed by immunohistochemical analysis of the lung, liver, and bone. Blood was collected at 2-week intervals by facial vein bleeding to monitor S100β levels in serum.

Charmsaz S., Hughes É., Bane F.T., Tibbitts P., McIlroy M., Byrne C., Cocchiglia S., McBryan J., Hennessy B.T., Dwyer R.M., Kerin M.J., Hill A.D, & Young L.S. (2017). S100β as a serum marker in endocrine resistant breast cancer. BMC Medicine, 15, 79.

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Dasatinib Modulates Inflamed Rheumatoid Arthritis FLS

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Human FLS harvested from patients with RA were purchased from Sigma Aldrich (St. Louis, Missouri, USA). In this study, the FLS-RA were pre-exposed to pro-inflammatory cytokine those are IL-1β and TNF-α and initiated inflammation in chondrocytes [15]. The FLS-RA cultures were incubated for overnight with serum starved medium (0.5% FCS). Serum-starved the FLS-RA were pre -stimulated with 5 ng/mL IL-1β and 10 ng/mL TNF-α for 24 h Sigma Aldrich (St. Louis, Missouri, USA) before being treated with dasatinib (Bristol-Myers Squibb, Istanbul, Turkey). After overnight, various concentrations (1 to 20 μM) of dasatinib were administered to induce FLS - RA cell cultures and incubated for 24 h. To investigate effect of dasatinib in inflamed cells was studied MTS assays (Cambridge, UK) and ELISA assays. MMP –1, –3, and –13 levels in FLS-RA culture were determined by ELISA (Cambridge, UK).

YALÇIN KEHRİBAR D., ÖZGEN M., YOLBAŞ S., YILDIRIM A., BAŞAK TÜRKMEN N., ÖNALAN ETEM E., ÇİFTÇİ O., ÖZERCAN İ.H, & KOCA S.S. (2021). The inhibition of Src kinase suppresses the production of matrix metalloproteinases in from synovial fibroblasts and inhibits MAPK and STATs pathways. Turkish Journal of Medical Sciences, 51(4), 2142-2149.

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Dasatinib Preparation Protocol

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For in vitro use, Dasatinib (Bristol-Myers Squibb) was dissolved in DMSO at a concentration of 10 mM and stored at -20°C. Subsequent dilutions were made in PBS immediately prior to use. For in vivo use, Dasatinib was dissolved in 80 mM citrate buffer and delivered by oral gavage at 0.01 mL/gram. A stock solution of 30 mg/mL was prepared weekly and stored at 4°C. Subsequent dilutions were made daily.

Hughes V.S, & Siemann D.W. (2018). Treatment with Src inhibitor Dasatinib results in elevated metastatic potential in the 4T1 murine mammary carcinoma model. Tumor & microenvironment, 1(1), 30-36.

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High-grade Glioma Cell Culture Assay

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For high-grade glioma primary cell cultures treatment assays, cells were passaged and plated in a 96-well plate at 2,000 cells/well in triplicate per condition. At 24 hours, cells were treated with chemotherapeutic agents, siRNA, or control, and assessed for viability 72 hours later using the Cell Titer Glo Assay (Promega) [28 (link)]. ON-TARGET PLUS siRNAs (GE Healthcare Dharmacon) against PDGFRA (J003162-11; J003162-12) and FGF2 (J006695-05; J006695-06) were used according to manufacturer's protocol. Chemotherapy was administered at a range of concentrations (0.01-1000 μM) based on previously published data: temozolomide (Sigma), CCNU (Sigma), Suberanilohydroxamic acid (SAHA), imatinib (Novartis), nilotinib (Novartis), and dasatinib (Bristol-Myers Squibb). Dose response curves were plotted using GraphPad Software, and IC₅₀ was calculated as the dose at which there was a 50% reduction in cell proliferation form untreated cells.

Koschmann C., Zamler D., MacKay A., Robinson D., Wu Y.M., Doherty R., Marini B., Tran D., Garton H., Muraszko K., Robertson P., Leonard M., Zhao L., Bixby D., Peterson L., Camelo-Piragua S., Jones C., Mody R., Lowenstein P.R, & Castro M.G. (2016). Characterizing and targeting PDGFRA alterations in pediatric high-grade glioma. Oncotarget, 7(40), 65696-65706.

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Kinase Inhibitor Sourcing in Research

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Rapamycin and LY294002 were from Calbiochem (Nottingham, U.K.), imatinib, dasatinib, and nilotinib were from Bristol-Myers Squibb (Princeton, New Jersey, USA) and Selleckchem (Newmarket, Suffolk, UK).

Pellicano F., Scott M.T., Helgason G.V., Hopcroft L.E., Allan E.K., Aspinall-O'Dea M., Copland M., Pierce A., Huntly B.J., Whetton A.D, & Holyoake T.L. (2014). The Antiproliferative Activity of Kinase Inhibitors in Chronic Myeloid Leukemia Cells Is Mediated by FOXO Transcription Factors. Stem Cells (Dayton, Ohio), 32(9), 2324-2337.

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Anticancer Drug Preparation and Storage

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Dasatinib (BMS-354825) was provided by Bristol-Myers-Squibb (Princeton, NJ). Docetaxel, gemcitabine, topotecan and doxorubicin were purchased from Sigma-Aldrich (St. Louis, MO). Docetaxel, gemcitabine, doxorubicin and Dasatinib were dissolved in dimethylsulfoxide (DMSO), and topotecan was dissolved in distilled water. Concentrated stock solutions were stored at −20°C.

Teoh D., Jia J., Nixon A.B., Grace L., Adams D.J., Murphy S.K, & Secord A.A. (2014). Dasatinib (BMS-35482) interacts synergistically with docetaxel, gemcitabine, topotecan and doxorubicin in ovarian cancer cells with high SRC pathway activation and protein expression. International journal of gynecological cancer : official journal of the International Gynecological Cancer Society, 24(2), 218-225.

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Protein Interactions in Cell Signaling

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Antibodies used were as follows: anti-Eps8, anti-paxillin, anti-GM130 and anti-p130Cas antibodies (BD Transduction Laboratories, NJ), anti-FAK, anti-pSrc Y416, anti-Src (clone 36D10), anti-LC3B, anti-GAPDH, anti-pPaxillin Y118 and anti-β-actin antibodies (Cell Signaling Technologies, Danvers, MA), as well as anti-FAK antibody conjugated to agarose (clone 4.47) (Millipore, Billerica, MA) and anti-LC3B for immunoprecipitations (MBL, Woburn, MA). The anti-TagCGYFP antibody was purchased from Evrogen (Cambridge, UK). TRITC–phalloidin was purchased from Life Technologies (Paisley, UK). Horseradish-peroxidase-conjugated secondary antibodies against rabbit or mouse IgG were purchased from Cell Signaling Technologies. Dasatinib was obtained from Bristol Myers Squibb (Princeton, NJ). The pEGFP-Eps8 1–821 and pEGFP-Eps8 1–535 constructs were a generous gift from Giorgio Scita (FIRC Institute of Molecular Oncology, Milan, Italy).

Schoenherr C., Serrels B., Proby C., Cunningham D.L., Findlay J.E., Baillie G.S., Heath J.K, & Frame M.C. (2014). Eps8 controls Src- and FAK-dependent phenotypes in squamous carcinoma cells. Journal of Cell Science, 127(24), 5303-5316.

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CML Primary Cell and LSC Treatments

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For experiments involving GSK343, CML and normal primary cells were cultured as above for the treatment regimens described below and in the text with media change every 3 days. For experiments involving treatment of LSCs with TKIs (imatinib (IM)/5µM, dasatinib (DAS)/150 nM and nilotinib (NIL)/5 µM; Bristol-Myers Squibb and Selleckchem) for up to 7 days, cells were grown in serum-free media without growth factors. The KCL22 cell line (CML, blast crisis; obtained from DSMZ cell bank in 2014; mycoplasma-negative; authenticated by DSMZ using RT-PCR for BCR-ABL1 expression and microsatellite repeat typing) was grown in RPMI 1640 (Sigma) supplemented with 10% fetal bovine serum, 2 mM L-glutamine and 1% penicillin-streptomycin. Experiments involving KCL22 cells were performed within 6 months from the date cells were obtained from DSMZ.

Scott M.T., Korfi K., Saffrey P., Hopcroft L.E., Kinstrie R., Pellicano F., Guenther C., Gallipoli P., Cruz M., Dunn K., Jorgensen H.G., Cassels J.E., Hamilton A., Crossan A., Sinclair A., Holyoake T.L, & Vetrie D. (2016). Epigenetic reprogramming sensitizes CML stem cells to combined EZH2 and tyrosine kinase inhibition. Cancer discovery, 6(11), 1248-1257.

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Preparation of TKI Stock Solutions

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Imatinib and nilotinib were provided by Novartis Pharma (Basel, Switzerland). Dasatinib was provided by Bristol-Myers Squibb (Princeton, NJ, USA). Stock solution of 100 mM Imatinib was prepared in sterile distilled water and stored at 4°C. Stock solutions of 10 mM nilotinib and 10 mM Dasatinib were prepared in dimethyl sulphoxide (Sigma-Aldrich, A3912 100) and stored in aliquots at −20°C.

Karvela M., Baquero P., Kuntz E.M., Mukhopadhyay A., Mitchell R., Allan E.K., Chan E., Kranc K.R., Calabretta B., Salomoni P., Gottlieb E., Holyoake T.L, & Helgason G.V. (2016). ATG7 regulates energy metabolism, differentiation and survival of Philadelphia-chromosome-positive cells. Autophagy, 12(6), 936-948.

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