in th17 cells

ML-209 is an antagonist of retinoic acid receptor-related orphan receptor γt (RORγt; IC50= 1.1 μM in a reporter assay).1It inhibits RORγt-induced transcription in HEK293T cells expressing the human receptor (IC50= 300 nM). ML-209 inhibits RORγt-dependent differentiation of isolated na?ve cord blood human CD4+T cells into Th17 T helper cells.

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

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).

4-Octylphenol is an endocrine disruptor with gender-specific effects on male germ cells, significantly reducing the mitotic index and the number of spermatogonia. It also causes inflammatory damage in the gills of carp by activating the complement system through the C3a C3a receptor (C3a C3aR) axis and C5a C5a receptor 1 (C5a C5aR1) axis. Furthermore, 4-Octylphenol induces immune suppression by disrupting the balance between helper T (Th) cells 1 Th2 and regulatory T (Treg) Th17 cells, and triggers inflammatory damage through the Toll-like receptor 7 (Toll-like Receptor (TLR)) inhibitor κBα nuclear factor κB (TLR7 IκBα NF-κB) pathway.

SR1555 is a selective RORγ inverse agonist that inhibits the development and function of TH17 cells, a subset of T cells that have been involved in the pathology of several autoimmune diseases such as rheumatoid arthritis and multiple sclerosis.

7β,27-dihydroxy Cholesterol is an oxysterol and agonist of retinoic acid receptor-related orphan receptor γ (RORγ) and RORγt. [1] It activates RORγ- or RORγt-dependent signaling with EC50 values of 691 and 1,045 nM, respectively, in reporter assays using HEK293T cells expressing the recombinant human receptors. 7β,27-dihydroxy Cholesterol is selective for RORγ and RORγt over a panel of eight additional nuclear receptors at 30 µM. It increases IL-17A production in Th17-polarized isolated human na ve CD4+ T cells when used at a concentration of 300 nM. 7β,27-dihydroxy Cholesterol (60 mg kg) increases IL-17A production in isolated mouse γδ T cells stimulated with 12-myristate 13-acetate and ionomycin .

RORγt inverse agonist 28 is a potent RORγt inverse agonist that regulates the differentiation of Th17 cells and inhibits IL-17 production, showing research potential in inflammatory and autoimmune diseases.

JAK1 TYK2-IN-3 is a selective, potent, orally active dual inhibitor of TYK2 (IC50: 6 nM) and JAK1 (IC50: 37 nM), with selective action on JAK2 (IC50: 140 nM) and JAK3 (IC50: 362 nM). It regulates the expression of TYK2 JAK1-related genes and formation of Th1, Th2, and Th17 cells to exert anti-inflammatory activity.

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.

JNJ-61803534 is a potent, orally active RORγt inverse agonist, demonstrating anti-inflammatory activity through inhibition of IL-17A production in human CD4+ T cells under Th17 differentiation conditions, with an IC50 of 9.6 nM.

AHR agonist 4 (compound 24e), as an Aryl hydrocarbon receptor (AHR) agonist, modulates the immune equilibrium between Th17 22 and Treg cells. It is a lead compound under investigation for anti-psoriasis drugs and demonstrates efficacy in mitigating imiquimod (IMQ)-induced psoriasis-like skin lesions [1].

NJK14047 inhibits p38 MAPK and prevents the differentiation of naive T-cells into Th1 and Th17 cells, thereby ameliorating collagen-induced rheumatoid arthritis and Imiquimod-induced psoriasis in mice [1].

SR1555 hydrochloride is the hydrochloride salt form of SR1555. It acts as an inverse agonist for the retinoic acid receptor-related orphan receptor γ (RORγ), with an IC50 of 1 μM. This compound inhibits the development and function of pro-inflammatory TH17 cells while increasing the frequency of anti-inflammatory regulatory T (Treg) cells. SR1555 hydrochloride is utilized in research related to autoimmune diseases.

G6PI 325-339 (human) effectively induces arthritis in B10.Q mice, primes Th1 and Th17 cells to cross-react with the murine G6PI protein, and triggers an arthritis model via a T and B cell-dependent pathway, although it operates without antibody effector mechanisms [1].