Famotidine hydrochloride

Famotidine (50 μM; 12 h) hydrochloride inhibits Histamine (HY-B1204)-induced TLR3 mRNA expression in A549 cells without affecting TLR7 expression; it also suppresses the cumulative upregulation of TLR3 expression in A549 cells co-treated with Histamine and poly (I:C) (HY-107202)^[1].
Famotidine (50 μM; 12 h preincubation, 1 h or 12 h poly (I:C) treatment) hydrochloride inhibits Histamine-enhanced TLR3-dependent activation of the TBK1/IRF3 and NF-κB pathways, and reduces the expression of downstream genes in poly (I:C)-treated A549 cells^[1].
Famotidine (50 μM; 12 h preincubation, 24 h SARS-CoV-2 infection) hydrochloride reduces the expression of TLR3 in SARS-CoV-2-infected Caco-2 cells, inhibits the Histamine-enhanced TLR3-dependent signaling pathway, and downregulates the mRNA levels of downstream inflammatory mediators; it also exerts an inhibitory effect on the Histamine-enhanced TLR3-dependent signaling pathway in SARS-CoV-2-infected Caco-2 cells^[1].
Famotidine hydrochloride is a selective inverse agonist and biased arrestin partial agonist for the human histamine H₂ receptor, with a binding affinity of 14 nM, an inverse agonist potency of 33 nM, and an EC₅₀ of 105 nM for arrestin recruitment. It does not exhibit significant interactions with H₁, H₃, or H₄ receptors^[2].
Famotidine hydrochloride induces a concentration-dependent, saturable increase in transepithelial electrical resistance (TEER) across Caco-2 cell monolayers via interaction with paracellular anion sites rather than tight junction tightening, reaching 193% of the control group at 25 mM^[5].
Famotidine hydrochloride undergoes apical-to-basolateral transport across Caco-2 cell monolayers via a combination of saturable facilitated diffusion and non-saturable passive diffusion, with its P_app value decreasing exponentially with concentration; it selectively inhibits the apical-to-basolateral transport of the cationic Ranitidine (HY-B0693) across Caco-2 cell monolayers, indicating that it targets cation-selective conductance via paracellular anion sites^[5].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.