Masitinib - CAS 790299-79-5
Catalog number: B0084-077384
Category: Inhibitor
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Masitinib is an orally bioavailable and multi-targeted protein tyrosine kinase inhibitor with potential antineoplastic activity.
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Catalog Number Size Price Stock Quantity
B0084-077384 250 mg $198 In stock
B0084-077384 500 mg $348 In stock
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AB-1010; AB 1010; AB1010; Masitinib. Brand name: Kinavet; Masivet.
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AB Science
1.Targeting mast cells in gastric cancer with special reference to bone metastases.
Leporini C1, Ammendola M1, Marech I1, Sammarco G1, Sacco R1, Gadaleta CD1, Oakley C1, Russo E1, De Sarro G1, Ranieri G1. World J Gastroenterol. 2015 Oct 7;21(37):10493-501. doi: 10.3748/wjg.v21.i37.10493.
Bone metastases from gastric cancer (GC) are considered a relatively uncommon finding; however, they are related to poorer prognosis. Both primary GC and its metastatic progression rely on angiogenesis. Several lines of evidence from GC patients strongly support the involvement of mast cells (MCs) positive to tryptase (MCPT) in primary gastric tumor angiogenesis. Recently, we analyzed infiltrating MCs and neovascularization in bone tissue metastases from primary GC patients, and observed a significant correlation between infiltrating MCPT and angiogenesis. Such a finding suggested the involvement of peritumoral MCPT by infiltrating surrounding tumor cells, and in bone metastasis angiogenesis from primary GC. Thus, an MCPT-stimulated angiogenic process could support the development of metastases in bone tissue. From this perspective, we aim to review the hypothetical involvement of tumor-infiltrating, peritumoral MCPT in angiogenesis-mediated GC cell growth in the bone microenvironment and in tumor-induced osteoclastic bone resorption.
2.Metallothionein-1G Facilitates Sorafenib Resistance through Inhibition of Ferroptosis.
Sun X1, Niu X1, Chen R2, He W1, Chen1, Kang R2, Tang D2. Hepatology. 2016 Mar 25. doi: 10.1002/hep.28574. [Epub ahead of print]
Hepatocellular carcinoma (HCC) is a major cause of cancer-related death worldwide and currently has the fastest rising incidence of all cancers. Sorafenib was originally identified as an inhibitor of multiple oncogenic kinases and remains the only approved systemic therapy for advanced HCC. However, acquired resistance to sorafenib has been found in HCC patients, which results in poor prognosis. Here, we showed that metallothionein (MT)-1G is a critical regulator and promising therapeutic target of sorafenib resistance in human HCC cells. The mRNA and protein expression of MT-1G is remarkably induced by sorafenib, but not other clinically-relevant kinase inhibitors (e.g., erlotinib, gefitinib, tivantinib, vemurafenib, selumetinib, imatinib, masitinib, and ponatinib). Activation of transcription factor nuclear factor erythroid 2-related factor 2 (NRF2), but not p53 and hypoxia-inducible factor 1-alpha (HIF1α), is essential for induction of MT-1G expression following sorafenib treatment.
3.Current Research Therapeutic Strategies for Alzheimer's Disease Treatment.
Folch J1, Petrov D2, Ettcheto M2, Abad S2, Sánchez-López E3, García ML3, Olloquequi J4, Beas-Zarate C5, Auladell C6, Camins A2. Neural Plast. 2016;2016:8501693. doi: 10.1155/2016/8501693. Epub 2016 Jan 3.
Alzheimer's disease (AD) currently presents one of the biggest healthcare issues in the developed countries. There is no effective treatment capable of slowing down disease progression. In recent years the main focus of research on novel pharmacotherapies was based on the amyloidogenic hypothesis of AD, which posits that the beta amyloid (Aβ) peptide is chiefly responsible for cognitive impairment and neuronal death. The goal of such treatments is (a) to reduce Aβ production through the inhibition of β and γ secretase enzymes and (b) to promote dissolution of existing cerebral Aβ plaques. However, this approach has proven to be only modestly effective. Recent studies suggest an alternative strategy centred on the inhibition of the downstream Aβ signalling, particularly at the synapse. Aβ oligomers may cause aberrant N-methyl-D-aspartate receptor (NMDAR) activation postsynaptically by forming complexes with the cell-surface prion protein (PrPC).
4.Tyrosine Kinase Inhibitor as a new Therapy for Ischemic Stroke and other Neurologic Diseases: is there any Hope for a Better Outcome?
Gągało I, Rusiecka I, Kocić I1. Curr Neuropharmacol. 2015;13(6):836-44.
The relevance of tyrosine kinase inhibitors (TKIs) in the treatment of malignancies has been already defined. Aberrant activation of tyrosine kinase signaling pathways has been causally linked not only to cancers but also to other non-oncological diseases. This review concentrates on the novel plausible usage of this group of drugs in neurological disorders, such as ischemic brain stroke, subarachnoid hemorrhage, Alzheimer's disease, multiple sclerosis. The drugs considered here are representatives of both receptor and non-receptor TKIs. Among them imatinib and masitinib have the broadest spectrum of therapeutic usage. Both drugs are effective in ischemic brain stroke and multiple sclerosis, but only imatinib produces a therapeutic effect in subarachnoid hemorrhage. Masitinib and dasatinib reduce the symptoms of Alzheimer's disease. In the case of multiple sclerosis several TKIs are useful, including apart from imatinib and masitinib, also sunitinib, sorafenib, lestaurtinib.
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CAS 790299-79-5 Masitinib

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