Motolimod | TLR8 agonist
NMR (Conforms)
Available Options
| Size: | Price | Quantity | |
|---|---|---|---|
| 5 mg | $80.00 | ||
| 25 mg | $295.00 |
Motolimod (926927-61-9) is a selective Toll-like receptor 8 (TLR8) agonist (EC50 = 100 nM). It stimulates the production of TNFα and IL-12 from monocytes and myeloid dendritic cells. Motolimod also stimulated IFNγ production from NK cells and increased their toxicity against K562 and ADCC by rituximab and trastuzumab.1,2 It induced apoptosis in monocytic myeloid-derived suppressor cells.3 Motolimod is being investigated in combination with other cancer immunotherapies.4,5 Motolimod has also been shown in induce secreted IL-1b and IL-8 via activation of the NLRP3 inflammasome.6
References/Citations:
1) Lu et al. (2012), VTX-2337 is a Novel TLR8 Agonist That Activates NK Cells and Augments ADCC; Clin. Cancer Res. 18 499
2) Lu et al. (2013), TLR8 agonist VTX-2337 enhances NKG2D-mediated cytotoxicity of NK cells; J. Immunother. Cancer 1 P44
3) Rutman et al. (2015), Motolimod,a selective TLR8 agonist, induces apoptosis in monocytic myeloid-derived suppressor cells (M-MDSC); J. Immunother. Cancer. 3 P296
4) Ferris et al. (2014), Active8: a random, double-blind, placebo-controlled study of chemotherapy plus cetuximab in combination with TLR8 agonist VTX-2337 in patients with recurrent or metastatic squamous cell carcinoma of the head and neck (SCCHN); J. Immunother. Cancer 2P69
5) Monk et al. (2017), Integrative Development of a TLR8 Agonist for Ovarian Cancer Chemo-Immunotherapy; Clin. Cancer Res. 23 1955
6) Dietsch et al. (2016), Coordinated Activation of Toll-Like Receptor8 (TLR8) and NLRP3 by the TLR8 Agonist, VTX-2337, Ignites Tumoricidal Natural Killer Cell Activity; PLoS One 11 e0148764
NMR (Conforms)
Safety Data Sheet:
Product Data Sheet:
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Motolimod (926927-61-9) is a selective Toll-like receptor 8 (TLR8) agonist (EC50 = 100 nM). It stimulates the production of TNFα and IL-12 from monocytes and myeloid dendritic cells. Motolimod also stimulated IFNγ production from NK cells and increased their toxicity against K562 and ADCC by rituximab and trastuzumab.1,2 It induced apoptosis in monocytic myeloid-derived suppressor cells.3 Motolimod is being investigated in combination with other cancer immunotherapies.4,5 Motolimod has also been shown in induce secreted IL-1b and IL-8 via activation of the NLRP3 inflammasome.6
References/Citations:
1) Lu et al. (2012), VTX-2337 is a Novel TLR8 Agonist That Activates NK Cells and Augments ADCC; Clin. Cancer Res. 18 499
2) Lu et al. (2013), TLR8 agonist VTX-2337 enhances NKG2D-mediated cytotoxicity of NK cells; J. Immunother. Cancer 1 P44
3) Rutman et al. (2015), Motolimod,a selective TLR8 agonist, induces apoptosis in monocytic myeloid-derived suppressor cells (M-MDSC); J. Immunother. Cancer. 3 P296
4) Ferris et al. (2014), Active8: a random, double-blind, placebo-controlled study of chemotherapy plus cetuximab in combination with TLR8 agonist VTX-2337 in patients with recurrent or metastatic squamous cell carcinoma of the head and neck (SCCHN); J. Immunother. Cancer 2P69
5) Monk et al. (2017), Integrative Development of a TLR8 Agonist for Ovarian Cancer Chemo-Immunotherapy; Clin. Cancer Res. 23 1955
6) Dietsch et al. (2016), Coordinated Activation of Toll-Like Receptor8 (TLR8) and NLRP3 by the TLR8 Agonist, VTX-2337, Ignites Tumoricidal Natural Killer Cell Activity; PLoS One 11 e0148764
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