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  • Imatinib Mesylate Raw Materials Imatinib Mesylate Powder

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    Product Overview:

    Imatinib mesylate inhibits Bcr-Abl tyrosine kinase at the cellular level both in vivo and ex vivo, and selectively inhibits the proliferation and induces apoptosis of fresh cells from Bcr-Abl-positive cell lineage cells, Ph chromosome-positive chronic granulocytic leukaemia and acute lymphoblastic leukaemia patients. In addition, imatinib mesylate inhibits platelet-derived growth factor (PDGF) receptor, stem cell factor (SCF), and c-Kit receptor tyrosine kinases, thereby inhibiting cellular behaviour mediated by PDGF and stem cell factor. Some patients can develop resistance through different mechanisms.

    Imatinib Mesylate Raw Materials Imatinib Mesylate Powder Attributes

    Imatinib Mesylate Raw Materials Imatinib Mesylate Powder

    CAS:220127-57-1

    MF:C30H35N7O4S

    Imatinib Mesylate

    MW:589.71

    EINECS:606-892-3

    Specification​: 99% min Imatinib Mesylate Powder

    Sample:Imatinib Mesylate Powder

    Packaging:1kg/bag, 25kg/drum

    Brand: Henrikang

    Appearance: White to Off-White

    Storage: Cool Dry Place

    Shelf Life: 2 Years

    Test Method: HPLC

    Imatinib Mesylate Raw Materials Imatinib Mesylate Powder Details

    Imatinib Mesylate Powder Usage and Synthesis.

    Imatinib mesylate is an antineoplastic agent . For the treatment of Philadelphia chromosome-positive chronic myeloid leukaemia (Ph+ CML) in the chronic, accelerated or acute phase.

    For the treatment of adult patients with unresectable and/or metastatic malignant gastrointestinal mesenchymal stromal tumours (GIST).

    In combination with chemotherapy for the treatment of paediatric patients with newly diagnosed Philadelphia chromosome-positive acute lymphoblastic leukaemia (Ph+ ALL).

    For the treatment of adult patients with relapsed refractory Philadelphia chromosome-positive acute lymphoblastic leukaemia (Ph+ ALL).

    Imatinib Mesylate Powder

    Uses of Imatinib Mesylate.

    1, For the treatment of Philadelphia chromosome-positive chronic myeloid leukaemia (Ph+CML) in the chronic, accelerated or acute phase.

    2, For the treatment of adult patients with unresectable and/or metastatic malignant gastrointestinal mesenchymal stromal tumour (GIST).

    3、Combination chemotherapy for the treatment of paediatric patients with newly diagnosed Philadelphia chromosome-positive acute lymphoblastic leukaemia (Ph+ALL).

    4, For the treatment of adult patients with relapsed refractory Philadelphia chromosome-positive acute lymphoblastic leukaemia (Ph+ALL).

    5. The safety and efficacy information for the following indications is mainly from foreign research data, with limited data on the Chinese population:

    (1) For the treatment of adult patients with eosinophilia syndrome (HES) and/or chronic eosinophilic leukaemia (CEL) with FIP1L1-PDGFRα fusion kinase.

    (2) For the treatment of adult patients with myelodysplastic syndromes/myeloproliferative disorders (MDS/MPD) with platelet-derived growth factor receptor (PDGFR) gene rearrangements.

    (3) For the treatment of aggressive systemic mast cell hyperplasia (ASM) in adult patients without D816V c-Kit gene mutation or unknown c-Kit gene mutation.

    (4) For the treatment of unresectable, recurrent or metastatic drusen fibrosarcoma of the skin (DFSP).

    (5) For adjuvant treatment of adult patients at significant risk of recurrence after surgical resection of Kit (CD117)-positive GIST. Patients at very low and low risk of recurrence should not receive this adjuvant therapy.

    Imatinib Mesylate

    Pharmacological Effects of Imatinib Mesylate.

    1. Imatinib is a small molecule protein tyrosine kinase inhibitor, which can effectively inhibit the activity of BCR-ABL tyrosine kinase (TK) as well as the following TK receptors: Kit, stem cell factor (SCF) receptor encoded through the c-Kit proto-oncogene, discoidal structural domain receptor (DDR1 and DDR2), colony-stimulating factor receptor (CSF-1R) and platelet-derived growth factor receptors α and β (PDGFR-α and PDGFR-β).

    Imatinib also inhibits cell behaviour mediated by activation of these receptor kinases.

    2, Imatinib inhibits BCR-ABL tyrosine kinase at the cellular level both in vivo and ex vivo, and selectively inhibits the proliferation and induces apoptosis of BCR-ABL-positive cell lineage cells, Philadelphia chromosome-positive (Ph+) chronic myelogenous leukaemia (CML), and fresh cells from patients with acute lymphoblastic leukaemia.

    3、Imatinib also inhibits platelet-derived growth factor (PDGF) receptor, stem cell factor (SCF), and tyrosine kinase of c-Kit receptor, thus inhibiting cellular behaviours mediated by PDGF and stem cell factor.

    4, Gastrointestinal interstitial tumour (GIST) cells express active Kit mutations, and in vitro experiments have shown that imatinib inhibits the proliferation and induces apoptosis in GIST cells.

    5, there are very few reports of resistance in the clinic, about the occurrence of imatinib resistance, the initial resistance (from the beginning of treatment that is ineffective) and secondary resistance is the difference between the whole process of exposure to imatinib shows ineffective, BCR-ABL tyrosine kinase, increased in the course of the disease process, that is, the molecular mechanism of the generation of drug resistance.

    Resistance has been observed to occur in patients taking too low a dose or not taking the drug regularly. Therefore, treatment should be initiated as early as possible, while the dose should be strictly adhered to.

    Imatinib Mesylate Raw Powder

    In vitro studies of Imatinib Mesylate.

    An in vitro assay for inhibition of tyrosine and serine/threonine protein kinases showed that Imatinib effectively inhibited V-Abl tyrosine kinase and PDGFR with IC50s of 0.6 μM and 0.1 μM, respectively.

    Imatinib inhibited SLF-dependent activation of wild-type c-kit kinase activity with an IC50 of approximately 0.1 μM, which is similar to the concentration required to inhibit PDGFR.

    Imatinib exhibited k inhibition of the human bronchial carcinoid cell line NCI-H727 and the human pancreatic carcinoid cell line BON-1 with IC50s of 32.4 μM and 32.8 μM, respectively.

    A recent study showed that Imatinib exerts its anti-leukaemic effect in chronic granulocytic leukaemia by down-regulating hERG1K(+) channels, which are highly expressed in leukaemic cells and exhibit favourable leukaemic appearance.

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