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     Blood cancers affect the production and function of your blood cells. Most of these cancers start in your bone marrow where blood is produced. Stem cells in your bone marrow mature and develop into three types of blood cells: red blood cells, white blood cells, or platelets. In most blood cancers, the normal blood cell development process is interrupted by uncontrolled growth of an abnormal type of blood cell. These abnormal blood cells, or cancerous cells, prevent your blood from performing many of its functions, like fighting off infections or preventing serious bleeding.

   There are three main types of blood cancers:

   ~Leukemia, a type of cancer found in your blood and bone marrow, is caused by the rapid production of abnormal white blood cells. The high number of abnormal white blood cells are not able to fight infection, and they impair the ability of the bone marrow to produce red blood cells and platelets.

   ~Lymphoma is a type of blood cancer that affects the lymphatic system, which removes excess fluids from your body and produces immune cells. Lymphocytes are a type of white blood cell that fight infection. Abnormal lymphocytes become lymphoma cells, which multiply and collect in your lymph nodes and other tissues. Over time, these cancerous cells impair your immune system.

   ~Myeloma is a cancer of the plasma cells. Plasma cells are white blood cells that produce disease- and infection-fighting antibodies in your body. Myeloma cells prevent the normal production of antibodies, leaving your body's immune system weakened and susceptible to infection. 

Cat. No. Product Name CAS No. Information



A potent, selective, orally available pan-PKC inhibitor with Ki of 0.22-3.2 nM for PKC isotypes; displays excellent selectivity against a broad panel of kinases (only GSK-3β IC50<1 uM); inhibits early T-cell activation with no general antiproliferative activity, also inhibits β2-integrin-mediated T-cell adhesiveness; prolongs rat heterotopic heart transplant survival in combination with adjunct immunosuppression agents.


TAK-659 hydrochloride


TAK-659 hydrochloride (Mivavotinib, TAK659) is a potent, selective and orally available SYK inhibitor with IC50 of 3.2 nM; displays 36, 42 and 23-fold selectivity over JAK3, ZAP70 and VEGFR2, respectively; also potently inhibits FLT-3; inhibits cellular proliferation in SYK-dependent DLBCL and FLT3-dependent AML cell lines, demonstrates potent tumor growth inhibition in the FLT3-dependent MV4-11 xenograft models.




LY-3214996 is a novel potent, selective, orally active ERK1/2 inhibitor with IC50 of 5 nM for both enzymes in biochemical assays; potently inhibits cellular phospho-RSK1 in BRAF and RAS mutant cancer cell lines; demonstrates inhibition of cell proliferation, general sensitivitity against tumor cells with MAPK pathway alterations including BRAF, NRAS or KRAS mutation; significantly inhibits tumor growth in vivo and is well tolerated in BRAF or NRAS mutant melanoma, BRAF or KRAS mutant colorectal, lung and pancreatic cancer xenografts or PDX models.




MAK683 (MAK-683) is a novel inhibitor of embryonic ectoderm development protein (EED) and allosteric inhibitor of polycomb repressive complex 2 (PRC2), selectively binds to the domain of EED that interacts with H3K27me3; leads to a conformational change in the EED H3K27me3-binding pocket and prevents the interaction of EED with the histone methyltransferase enhancer zeste homolog 2 (EZH2), inhibits tumor cell proliferation in EZH2-mutated and PRC2-dependent cancer cells.


Tipifarnib S enantiomer


Tipifarnib S enantiomer is a potent and selective inhibitor of FTase (farnesyltransferase); inhibits the farnesylation of lamin B and K-RasB peptide substrates with IC50s of 0.86 nM and 7.9 nM, respectively; no activity for PGGT1(IC50>50 uM); shows sensiticity for tumor cell lines bearing H-ras or N-ras mutations; inhibits the growth of tumors bearing mice and orally bioavailable.




A potent type II JAK2 inhibitor; inhibits the proliferation of SET2 JAK2 V617F cells (GI50=59 nM); reverses type I JAK inhibitor persistence and demonstrates efficacy in myeloproliferative neoplasms; reduces mutant allele burden in vivo, shows significant efficacy in Jak2V617F-driven polycythemia vera; orally active.




A highly potent and orally bioavailable small-molecule inhibitor of Menin-MLL interaction with Kd of 9.3 nM; effectively induces differentiation of MLL leukemia cells and and substantially increases expression of CD11b, also reduces expression of Hoxa9 and Meis1; induces marked anti-proliferative effects in MV4;11 cells with GI50 of 200 nM; blocks hematologic tumors in vivo and reduces MLL leukemia tumor burden in mouse models.




eFT508 (Tomivosertib) is a potent, highly selective, reversible, ATP-competitive, and orally bioavailable MNK1 and MNK2 inhibitor with IC50 of 1-2 nM in enzyme assays; dose-dependently reduces eIF4E phosphorylation at Serine 209 in tumor cell lines with IC50 of 2-16 nM; shows anti-proliferative activity against multiple DLBCL cell lines, decreases the production of pro-inflammatory cytokines including TNFα, IL-6, IL-10 and CXCL10; demonstrates significant anti-tumor activity in human lymphoma xenograft models which harbor activating MyD88 mutations.


PIM-447 dihydrochloride


A highly potent and selective inhibitor of pan-Pim with IC50s of 6/18/9 pM for Pim/1/2/3 respectively; induces apoptosis by a decrease in phospho-Bad Ser112 and c-Myc levels and the inhibition of mTORC1 pathway; significantly reduces the tumor burden and prevents tumor-associated bone loss in a murine model of human myeloma.




BAY-1436032 (BAY1436032) is a potent, selective, orally available inhibitor of pan-mutant IDH1 with IC50 of 15 nM for both IDH1 R132H and R132C, respectively; shows no effect on wild-type IDH1; strongly reduces 2-HG levels in cells carrying IDH1-R132H, -R132C, -R132G, -R132S and -R132L mutations; significantly prolongs survival of mice intracerebrally transplanted with human astrocytoma carrying the IDH1R132H mutation.

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