Hello Sandy, I think what you are referring to is FLT-3 it is a kinase that is found to be active in certain types of leukemia, such as CML and AML. Both c- kit and FLT-3 are kinases that are active in CML. Gleevec targets c- kit, but not FLT-3, if I am not mistaken. It just may be that this young person you mention here has had molecular or gene testing and his doctors feel that treatment with a drug that inhibits FLT-3 would be better suited to him.
I have pasted an article from a news release in November 2004 that indicates that a biotech company has signed a licensing agreement with Novartis to develop this molecule and bring it to market. You should keep us posted on how well this works for this patient. By the way, his mother donated "stem cells" for the BMT. I am sorry that he has relapsed and hopefully this drug regimen will help him. Best, Cheryl-Anne Novartis Selects Drug Candidate for Clinical Development from Protein Kinase Research Collaboration with Vertex --Novel compound, VX-322, targets key mechanisms implicated in leukemia and other cancers-- Cambridge, MA, November 10, 2004 -- Vertex Pharmaceuticals Incorporated (Nasdaq: VRTX) today announced that Novartis has selected a small molecule protein kinase inhibitor, VX-322, from Vertex for clinical development for the treatment of cancer. VX-322 is the first drug candidate to be transferred from Vertex to Novartis under an amended agreement to discover and develop drug candidates directed at the protein kinase gene family, and represents a novel, highly targeted approach to the treatment of cancer. In conjunction with the selection of VX-322, Vertex will receive $10 million from Novartis, a portion of which will be recognized by Vertex as revenue in the fourth quarter of 2004, with the remainder recognized through the term of the contract. "Vertex's delivery of this innovative drug candidate highlights our progress in drug discovery on many promising molecular targets in the kinase gene family, as well as the continued strength of the research collaboration between Novartis and Vertex," said Peter Mueller, Ph.D., Senior Vice President of Drug Discovery and Innovation and Chief Scientific Officer at Vertex. "VX-322 represents a novel approach to address key molecular mechanisms that drive tumor growth, and we are pleased that it has been selected for development by Novartis, an industry leader in cancer drug development." VX-322 is a potent, selective, dual inhibitor of the Flt-3 and c-kit kinases, which function as molecular switches that regulate the growth of certain cancers. Flt-3 inhibition has attracted significant attention among cancer researchers as a highly targeted approach to the treatment of certain leukemias as well as other hematological malignancies and solid tumors. Flt-3 is abnormally activated or upregulated in a wide range of leukemias, including more than 70% to 100% of patients with acute myelogenous leukemia (AML). Current treatment for AML generally involves aggressive chemotherapy with "non-specific" agents that cannot discriminate between healthy and diseased cells, which results in significant toxicity and limited efficacy. The five-year survival rate for AML patients is 14%. New targeted approaches hold the potential to transform the treatment of AML: reducing side effects, improving tolerability and increasing the efficacy of chemotherapeutic regimens. In May 2000, Vertex and Novartis entered an alliance to discover, develop and commercialize small molecule drugs directed at targets in the kinase protein family. The agreement was amended in February 2004, providing for a more rapid and earlier stage transfer of the drug candidates discovered by Vertex to Novartis for clinical development. Upon selection, Novartis holds worldwide development and commercialization rights to VX-322. Vertex will receive milestone payments based on clinical advancement of VX-322, and will receive royalties based on commercial sales. Background Information: Flt-3 and c-kit Kinases, and Discovery of VX-322 VX-322 was discovered in a joint effort by scientists in Vertex's San Diego and Cambridge research sites, leveraging expertise in protein biochemistry, structural biology, high throughput cell assays and medicinal chemistry. Earlier in 2004, Vertex researchers published the three-dimensional atomic crystal structure of Flt-3 in the scientific journal Molecular Cell1, a key scientific advance that provided insight into the mechanism by which mutated forms of the Flt-3 receptor can activate themselves, triggering uncontrolled proliferation of immature blood cells characteristic in several types of leukemia. Flt-3 kinase is abnormally activated or upregulated in the majority of patients with AML, as well as in patients with acute lymphoblastic leukemia (ALL) and chronic myelogenous leukemia (CML). Specific Flt-3 mutations that are believed to be key drivers of cell proliferation are present in up to 40% of AML patients. In addition, the protein c-kit has been found at high levels in 60% to 80% of AML patients. Preclinical studies conducted at Vertex using cells isolated from AML patients have suggested that dual Flt-3/c-kit inhibition provides more potent reduction in cell proliferation compared to inhibitors of Flt-3 or c-kit kinase alone. These data have enabled researchers to design molecules with optimized inhibitory profiles against Flt-3 and c-kit kinases. Key Facts About Leukemia Leukemia is a cancer of the blood characterized by uncontrolled growth and proliferation of cells in bone marrow, the tissue responsible for the production of all blood cells. According to the Leukemia and Lymphoma Society, an estimated 33,440 individuals will be diagnosed with leukemia in the U.S. in 2004, more than one third of whom will have acute myelogenous leukemia (AML), the most common form. --- In [email protected], Sandy Johnson <[EMAIL PROTECTED]> wrote: > > Hello,Doe's anyone know what fit 3 drug is? We know a 12 year old boy that is going to start on this in Feb.That is as soon as the Doctor can get it for him.He is in St.Judes.He had a bmt that failed.His Mother gave him some kind of cells not sure what that was,and they have him on hydrea for now.His name is Nolen Kane,he could use a lot of prayers right now.Sandy > > > --------------------------------- > Yahoo! Photos > Ring in the New Year with Photo Calendars. Add photos, events, holidays, whatever. > New! 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