Nangibotide TFA is a synthetic peptide that specifically inhibits the TREM‐1 (triggering receptor expressed on myeloid cells‐1) pathway by acting as a decoy receptor to block its activation. It reduces excessive inflammation, restores vascular function, and improves survival in animal models of septic shock.

Nangibotide TFA is a synthetic peptide that specifically inhibits the TREM‐1 (triggering receptor expressed on myeloid cells‐1) pathway by acting as a decoy receptor to block its activation. It reduces excessive inflammation, restores vascular function, and improves survival in animal models of septic shock.

Nangibotide TFA is a synthetic peptide that specifically inhibits the TREM‐1 (triggering receptor expressed on myeloid cells‐1) pathway by acting as a decoy receptor to block its activation. It reduces excessive inflammation, restores vascular function, and improves survival in animal models of septic shock.

Jagged-1 (188-204) (TFA) is a peptide fragment of the Jagged-1 (JAG-1) protein with Notch agonist activity. JAG-1 is highly expressed in cultured and primary multiple myeloma (MM) cells. JAG-1 also induces the maturation of monocyte-derived human dendritic cells.

Jagged-1 (188-204) (TFA) is a peptide fragment of the Jagged-1 (JAG-1) protein with Notch agonist activity. JAG-1 is highly expressed in cultured and primary multiple myeloma (MM) cells. JAG-1 also induces the maturation of monocyte-derived human dendritic cells.

Jagged-1 (188-204) (TFA) is a peptide fragment of the Jagged-1 (JAG-1) protein with Notch agonist activity. JAG-1 is highly expressed in cultured and primary multiple myeloma (MM) cells. JAG-1 also induces the maturation of monocyte-derived human dendritic cells.

Jagged-1 (188-204) (TFA) is a peptide fragment of the Jagged-1 (JAG-1) protein with Notch agonist activity. JAG-1 is highly expressed in cultured and primary multiple myeloma (MM) cells. JAG-1 also induces the maturation of monocyte-derived human dendritic cells.

Icotrokinra (JNJ-77242113, JNJ-2113, PN-235) is an orally available and selective antagonist of the IL-23 receptor. It also inhibits IL-23–induced STAT3 phosphorylation in peripheral blood mononuclear cells with an IC50 of 5.6 pM and suppresses IL-23–induced IFN-γ production in NK cells with an IC50 of 18.4 pM. It also exhibits anti-inflammatory activity in a TNBS-induced colitis […]

Icotrokinra (JNJ-77242113, JNJ-2113, PN-235) is an orally available and selective antagonist of the IL-23 receptor. It also inhibits IL-23–induced STAT3 phosphorylation in peripheral blood mononuclear cells with an IC50 of 5.6 pM and suppresses IL-23–induced IFN-γ production in NK cells with an IC50 of 18.4 pM. It also exhibits anti-inflammatory activity in a TNBS-induced colitis […]

Icotrokinra (JNJ-77242113, JNJ-2113, PN-235) is an orally available and selective antagonist of the IL-23 receptor. It also inhibits IL-23–induced STAT3 phosphorylation in peripheral blood mononuclear cells with an IC50 of 5.6 pM and suppresses IL-23–induced IFN-γ production in NK cells with an IC50 of 18.4 pM. It also exhibits anti-inflammatory activity in a TNBS-induced colitis […]