4 Results for "

TNF-α-IN-10

" in MedChemExpress (MCE) Product Catalog:
Products (4)

4 Results for "TNF-α-IN-10" in MCE Product Catalog:

Cat. No.: HY-153330
CAS No.: 2247720-56-3
Research Areas:  

Inflammation/Immunology

TNF-α-IN-10 (compound 8a) is a IL-6 and TNF-α inhibitor. TNF-α-IN-10 shows anti-inflammatory activity .
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14
14 Cited Publications
Cat. No.: HY-110353
CAS No.: 1821387-73-8
Purity:  99.96%
Research Areas:  

Inflammation/Immunology Cancer

CU-T12-9 is a specific TLR1/2 agonist with EC50 of 52.9 nM in HEK-Blue hTLR2 SEAP assay. CU-T12-9 activates both the innate and the adaptive immune systems. CU-T12-9 selectively activates the TLR1/2 heterodimer, not TLR2/6. CU-T12-9 signals through NF-κB and invokes an elevation of the downstream effectors TNF-α, IL-10, and iNOS .
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Cat. No.: HY-168384
CAS No.: 875158-73-9
M04 is an agonist of STING. It induces the expression of the IFN reporter gene in HEK293T cells expressing wild-type human STING, but does not induce this expression in HEK293T cells expressing the R71H-G230A-R293Q (HAQ) STING variant or in mouse RAW 264.7 cells, indicating that its activity is dependent on allelic and species variations. M04 induces the production of TNF-α, IL-10, IL-1β, and IL-12p70 in human peripheral blood mononuclear cells (PBMCs). At a concentration of 50 µM, M04 stimulates dendritic cells isolated from PBMCs to express the MHC class II cell surface receptor HLA-DR and co-stimulatory molecules CD40, CD80, and CD86, and also enhances their ability to activate T cells in an ex vivo assay. M04 can be used in research on inflammatory immune diseases .
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Cat. No.: HY-110353R
CAS No.: 1821387-73-8
CU-T12-9 (Standard) is the analytical standard of CU-T12-9 (HY-110353). This product is intended for research and analytical applications. CU-T12-9 is a specific TLR1/2 agonist with EC50 of 52.9 nM in HEK-Blue hTLR2 SEAP assay. CU-T12-9 activates both the innate and the adaptive immune systems. CU-T12-9 selectively activates the TLR1/2 heterodimer, not TLR2/6. CU-T12-9 signals through NF-κB and invokes an elevation of the downstream effectors TNF-α, IL-10, and iNOS .
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