TLR8 agonist 10
TLR8 agonist 10 is a selective TLR8 agonist with an EC50 of 0.019 μM in humans. TLR8 agonist 10 activates TLR8-mediated signaling pathways. As a latency-reversing agent, TLR8 agonist 10 reactivates latent HIV-1 reservoirs. TLR8 agonist 10 activates innate cytotoxic natural killer cells to target HIV-infected CD4+ T cells. TLR8 agonist 10 is applicable to research related to HIV-1 infection.
Nur für Forschungszwecke. Wir verkaufen nicht an Patienten.
- CAS. Nr.: 2796210-93-8
- Formel: C20H30N4
- Molecular Weight:326.48
-
Speicherung:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biologische Aktivität
Beschreibung
IC50 & Target
|
HIV-1 |
hTLR8 0.019 μM (IC50) |
In Vitro
TLR8 agonist 10 (Compound 23A) (0-10 μM) potently reactivates latent HIV-1 in U1 cells in vitro without significant cytotoxicity[1].
TLR8 agonist 10 (0-10 μM) can indirectly activate latent HIV-1 in ACH-2 cells via cytokine signals produced by treated human PBMCs, and exhibits no significant cytotoxicity against ACH-2 cells[1].
TLR8 agonist 10 (0-10 μM) potently reactivates latent HIV-1 in OM10.1 cells in a concentration-dependent manner, with no significant cytotoxicity[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Parmacokinetics
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Chemical Information
-
CAS. Nr. 2796210-93-8
-
Molecular Weight 326.48
-
Formel C20H30N4
-
SMILES
CCCCNC1=CC(CC2=CC=C(C=C2)CN(C)C)=C(N=C1N)C
-
Versand
Room temperature in continental US; may vary elsewhere.
-
Speicherung
Please store the product under the recommended conditions in the Certificate of Analysis.
Protokoll
-
Research Protocol for Infectious Diseases
Infectious-disease experiments test how pathogens interact with host barriers, innate immune receptors, inflammatory signaling, pathogen replication, and tissue injury; pattern-recognition receptors such as TLRs, RIG-I-like receptors, NOD-like receptors, and inflammasomes detect microbial molecules and activate NF-κB, interferon, and cytokine responses. The central hypothesis is that infection severity reflects the balance between pathogen burden and host response: protective inflammation restricts pathogen growth, whereas excessive or mislocalized inflammation contributes to tissue damage and disease phenotype. Unresolved questions include which host pathways are protective versus pathogenic, why some infection models fail to translate to human disease, and which combined readouts best predict clinically relevant infection outcomes.
-
Cell Viability Determination by MTT Colorimetric Assay
The following protocol uses the MTT colorimetric assay as a classic literature-established method for assessing cell viability/metabolic activity in cultured mammalian cells. MTT[3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] is reduced by metabolically active cells to a colored formazan product; the amount of formazan is quantified spectrophotometrically and provides an indirect measure of metabolically active viable cells. Importantly, MTT reduction reflects cellular oxidoreductase/metabolic activity rather than an absolute direct count of living cells, so changes in cellular metabolism can alter the signal independently of cell number.
Reinheit & Dokumentation
Verweise
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)