Talmapimod

Talmapimod (SCIO-469) is an orally active and selective inhibitor of p38α MAPK with an IC50 of 9 nM. Talmapimod inhibits the secretion of inflammatory factors (such as TNFα, IL-1β, IL-6, and VEGF) by suppressing the p38α MAPK pathway, and it also inhibits angiogenesis and osteoclast activation. Talmapimod inhibits the growth of multiple myeloma cells and induces apoptosis. Talmapimod can be used to study various hematological malignancies (such as multiple myeloma, myelodysplastic syndrome) [1][2][3][4].

Product Specifications

CAS Number

[309913-83-5]

Product Name Alternative

SCIO-469

UNSPSC

12352005

Target

Apoptosis; Interleukin Related; p38 MAPK; TNF Receptor; VEGFR

Type

Reference compound

Related Pathways

Apoptosis; Immunology/Inflammation; MAPK/ERK Pathway; Protein Tyrosine Kinase/RTK

Applications

Cancer-Kinase/protease

Field of Research

Cancer; Inflammation/Immunology; Metabolic Disease; Neurological Disease

Assay Protocol

https://www.medchemexpress.com/SCIO-469.html

Concentration

10mM

Purity

98.68

Solubility

DMSO : ≥ 100 mg/mL

Smiles

O=C(N(C)C)C(C1=CN(C)C2=C1C=C(C(N3[C@H](C)CN(CC4=CC=C(F)C=C4)[C@@H](C)C3)=O)C(Cl)=C2)=O

Molecular Formula

C27H30ClFN4O3

Molecular Weight

513.00

References & Citations

[1]Hideshima T et al. p38 MAPK inhibition enhances PS-341 (bortezomib) -induced cytotoxicity against multiple myeloma cells. Oncogene. 2004 Nov 18, 23 (54), 8766-76.|[2]Vanderkerken K et al. Inhibition of p38alpha mitogen-activated protein kinase prevents the development of osteolytic bone disease, reduces tumor burden, and increases survival in murine models of multiple myeloma. Cancer Res. 2007 May 15;67 (10) :4572-7.|[3]Navas T, et al. Inhibition of p38alpha MAPK disrupts the pathological loop of proinflammatory factor production in the myelodysplastic syndrome bone marrow microenvironment. Leuk Lymphoma. 2008 Oct;49 (10) :1963-75.|[4]Medicherla S, et al. p38alpha-selective MAP kinase inhibitor reduces tumor growth in mouse xenograft models of multiple myeloma. Anticancer Res. 2008 Nov-Dec;28 (6A) :3827-33.