Motolimod_926927-61-9_DataSheet_MedChemExpress

Motolimod_926927-61-9_DataSheet_MedChemExpress

Product Name:

Motolimod CAS No.:

926927-61-9Cat. No.:

HY-13773MWt:

458.60Formula:

C28H34N4O2Purity :>98%

Solubility:Mechanisms:

Biological Activity:

References:

Caution: Not fully tested. For research purposes only

Medchemexpress LLC

https://www.360docs.net/doc/6015761418.html,

[1]. Lu H, et al. VTX-2337 is a novel TLR8 agonist that activates NK cells and augments ADCC. Clin Cancer

Res. 2012 Jan 15;18(2):499-509.[2]. Stephenson RM, et al. TLR8 stimulation enhances cetuximab-mediated natural killer cell lysis of head and neck cancer cells and dendritic cell cross-priming of EGFR-specific CD8+ T cells. Cancer Immunol

Immunother. 2013 Aug;62(8):1347-57.[3]. Brueseke TJ, et al. Toll-like receptor 8: augmentation of innate immunity in platinum resistant ovarian

carcinoma. Clin Pharmacol. 2013 May 23;5:13-9.Motolimod(VTX-2337) is a small-molecule Toll-like receptor 8 (TLR8) agonist with potential

immunostimulating and antineoplastic activities.

IC50 value: 100 nM(EC50) [1]

Target: TLR8 agonist VTX-2337 selectively activates TLR8 with an EC(50) of about 100 nmol/L and stimulates production of TNF αand interleukin (IL)-12 from monocytes and myeloid dendritic cells (mDC). VTX-2337 stimulates IFN γ

production from NK cells and increases the cytotoxicity of NK cells against K562 and ADCC by rituximab and trastuzumab. Effects of VTX-2337 on NK cells were, in part, from direct activation as increased IFN γproduction and cytotoxic activity were seen with purified NK cells. Finally, VTX-2337 augments ADCC by rituximab in PBMCs with different Fc γR3A genotypes (V/V, V/F, and F/F at position 158). VTX-2337 is a novel small-molecule TLR8 agonist that activates monocytes, DCs, and NK c...

Pathways:Immunology/Inflammation; Target:TLR Product Data Sheet

10 mM in DMSO

11 D e e r P a r k D r i v e , S u i t e 102D M o n m o u t h J u n c t i o n , N J 08852,U S A

E m a i l : i n f o @m e d c h e m e x p r e s s .c o m W e b : w w w .m e d c h e m e x p r e s s .c o m

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