th17 cell

GSK805 is a potent, orally bioavailable and CNS-penetrant RORγt inhibitor.

ROR agonist-1 is a potent and orally bioavailable inverse agonist of the retinoic acid receptor-related orphan receptor C2 (RORC2), demonstrating inhibition of IL-17A production from human primary TH17 cells with a pIC50 of 7.5.

TMP778 is an effective and selective RORγt inverse agonist (IC50: 7 nM in FRET assay).

3-Oxo-5β-cholanoic acid (Dehydrolithocholic acid) is a bile acid metabolite that inhibits TH17 cell differentiation by directly binding to the transcription factor RORγt with a Kd of 1.13 μM.

Ciglitazone (ADD 3878) is a potent and selective PPARγ agonist (EC50: 3 μM) and oral hypoglycemic agent. Ciglitazone inhibits proliferation and differentiation of th17 cells, decreases insulin levels, vascular endothelial growth factor production and blood pressure, and induces cell cycle arrest in gastric cancer cells. Selegiline induces apoptosis in opossum kidney epithelial cells and activates nuclear translocation of p38 MAPK and apoptosis-inducing factor (AIF). Ciglitazone exhibits hypoglycaemic activity in animal models of obesity and hyperglycaemia.

AJI-100 serves as a dual-target inhibitor, effectively blocking Aurora kinase A and JAK2, with respective IC50 values of 12.7 nM and 18.5 nM. It inhibits T cell mitosis and cell polarity by directly targeting Aurora kinase A and reduces STAT3 phosphorylation by inhibiting JAK2 activation, consequently diminishing the differentiation of TH1 and TH17 cells. This compound is utilized in researching immune response regulation and the prevention of graft-versus-host disease (GVHD).

AJI-214 functions as a dual-target inhibitor that specifically blocks Aurora kinase A and JAK2. By directly inhibiting Aurora kinase A, AJI-214 prevents mitotic progression and cell polarity in T cells while concurrently suppressing JAK2 activation to reduce STAT3 phosphorylation. This inhibition decreases the differentiation of TH1 and TH17 cells. AJI-214 is utilized in research focused on the modulation of immune responses and the prevention of graft-versus-host disease (GVHD).

ITK-IN-6 is a potent and selective ITK inhibitor (Kd = 387 nM). It binds directly to the ITK kinase domain. This compound prevents the release of pro-inflammatory cytokines and the activation and differentiation of Th2 and Th17 cells. ITK-IN-6 improves asthma progression by reducing inflammatory cell infiltration, mucus production, and IgE generation. It significantly inhibits airway inflammation and is used in asthma research.

KB-0118 (BBC0115) is an inhibitor targeting the BET bromodomain. It selectively binds to BRD2 and BRD4, with dissociation constants (Kd) of 36.7 μM for BRD2 BD1 and 47.4 μM for BRD4 BD1, while not binding to BRD3. KB-0118 suppresses the secretion of pro-inflammatory cytokines such as TNF, IL-1β, and IL-23a, and selectively inhibits Th17 cell differentiation. The compound regulates Th17-driven inflammation through the epigenetic suppression of BRD4, as evidenced by the downregulation of STAT3 and BRD4 target genes. Additionally, KB-0118 exhibits immunomodulatory effects in inflammatory bowel disease (IBD) models.

Lithocholic acid 3-sulfate disodium (Sulfolithocholic acid disodium) acts as a RORgammat ligand and inhibits Th17 cell differentiation.Lithocholic acid 3-sulfate disodium is a sulfated product of lithocholic acid (LCA) and induces a decrease in arterial blood pressure. Lithocholic acid 3-sulfate disodium is a sulfated product of lithocholic acid (LCA) that induces cellular damage.

SR12418 is a specific synthetic ligand for REV-ERB, demonstrating binding affinity for both REV-ERBα (IC50 = 68 nM) and REV-ERBβ (IC50 = 119 nM) in TR-FRET assays. SR12418 inhibits IL-17A expression in EL4 cells and suppresses TH17 cell differentiation, making it suitable for studies on experimental autoimmune encephalomyelitis (EAE) and colitis.

RORγt agonist 3 is a potent agonist of RORγt that induces Th17 cell differentiation, increases levels of pro-inflammatory cytokines, and enhances lymphocyte cytotoxicity. Moreover, [it] blocks the production of regulatory T cells and suppresses the immune response.

RORγt agonist 2 is a potent agonist of RORγt that induces Th17 cell differentiation, increases levels of pro-inflammatory cytokines, and enhances lymphocyte cytotoxicity. It exhibits an inhibitory effect on the production of regulatory T cells and can suppress immune responses.

Vimirogant (VTP-43742) hydrochloride is an orally active, selective RORγt inhibitor (IC50: 17 nM, Ki: 3.5 nM) that is more than 1000 times more selective than RORα and RORβ. It inhibits Th17 differentiation and IL-17A secretion in mouse spleen cells with an IC50 of 57 nM and does not affect Th1, Th2, or Treg cell differentiation.

RORγt inverse agonist 26, a potent reverse agonist of RORγt, effectively modulates Th17 cell differentiation and suppresses IL-17 production. This compound shows promising potential for researching inflammation and autoimmune diseases.

BET BD2-IN-1 (compound 45) is a potent and selective BET BD2 inhibitor with an IC50 value of 1.6 nM. It suppresses Th17 cell differentiation by reducing the activation of STAT3 and NF-κB, making it relevant for psoriasis and inflammatory bowel disease (IBD) research [1].

SHR0302 (ARQ252) is a JAK inhibitor that binds JAK1 with stronger affinity than others (Selectivity for JAK1 is more than 10 times for JAK2, 77 times for JAK3, 420 times for Tyk2).

Ciglitazone (Standard) is the standard substance of Ciglitazone, and it is applicable for quantitative analysis, quality control, and related research in biochemical experiments. Ciglitazone (ADD 3878) is a potent and selective PPARγ agonist (EC50: 3 μM) and oral hypoglycemic agent. Ciglitazone inhibits proliferation and differentiation of th17 cells, decreases insulin levels, vascular endothelial growth factor production and blood pressure, and induces cell cycle arrest in gastric cancer cells. Selegiline induces apoptosis in opossum kidney epithelial cells and activates nuclear translocation of p38 MAPK and apoptosis-inducing factor (AIF). Ciglitazone exhibits hypoglycaemic activity in animal models of obesity and hyperglycaemia.

G6PI 325-339 (human) is an effective reagent for inducing arthritis in B10.Q mice. It triggers cross-reactive Th1 and Th17 cell responses against the mouse G6PI protein and can be used to induce an arthritis model through T and B cell-dependent pathways, although it does not involve antibody-mediated mechanisms.

G6PI 325-339 (human) hydrochloride is an effective inducer of arthritis in B10.Q mice. It triggers cross-reactivity of Th1 and Th17 cells with mouse G6PI protein. This compound induces an arthritis model through T and B cell-dependent pathways, without involving any antibody effector mechanisms.