AS2863619 

AS2863619 GMP is AS2863619 (HY-126675) produced by using GMP guidelines. GMP small molecules works appropriately as an auxiliary reagent for cell therapy manufacture. AS2863619 is an orally active CDK8/19 inhibitor that also inhibits BMP2, MDA5 and RIG-I receptors. AS2863619 targets Stat5a-CDK8/19 to promote the differentiation of CD4⁺ T cells into regulatory T cells and induce FOXP3 expression, thereby restoring immune homeostasis and establishing transplant immune tolerance. AS2863619 also enhances the BMP2/SMAD signaling pathway to promote osteogenic differentiation and inhibit adipogenic differentiation. AS2863619 exerts osteoprotective effects by alleviating inflammation-induced impairment of osteogenic function and inducing neutrophil apoptosis (apoptosis). AS2863619 can be applied to research in related fields such as periodontitis-induced bone defects^[1][2][3].

AS2863619 GMP, combination with IL-2 and TGF-β, enhances the differentiation of primary CD4+ T cells isolated from the spleens of DBA/1 mice into Treg, and its efficacy is superior to that of the regimens using IL-2 alone combined with either TGF-β or AS2863619^[1].
AS2863619 GMP (125 nM-2 μM; 7-10 d) enhances osteogenic differentiation of human periodontal ligament stem cells, with concentrations of 250 nM and 500 nM increasing ALP activity, upregulating key osteogenic markers, and accelerating mineralized nodule formation on day 10^[2].
AS2863619 GMP (250 nM-500 nM; 7-21 d) inhibits adipogenic differentiation of human periodontal ligament stem cells by reducing lipid droplet formation and downregulating key adipogenic genes^[2].
AS2863619 GMP (250 nM-500 nM; 7-10 d) alleviates rhTNF-α-induced osteogenic differentiation impairment of human periodontal ligament stem cells by inhibiting the RIG-I/MDA5 receptor-mediated RLR signaling pathway, and the 500 nM concentration reverses the inflammatory impairment blocked by the RLR agonist Poly (I:C)^[2].
Combination of AS2863619 GMP (1 mM/mL; 5 d) with IL-2 and TGF-β₁ induces transdifferentiation of allogeneic antigen-specific Balb/c CD4⁺ T cells into ag-Treg, while upregulating the expression of Treg-specific genes and enriching pathways associated with T cell tolerance induction^[3].
AS2863619 GMP (0.01-10 μM; 2 h) significantly increases the apoptosis level of human polymorphonuclear neutrophils (PMNs) stimulated by IC, with a value comparable to that of the negative control group, while it does not significantly reduce cell viability^[4].

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

AS2863619 GMP (30 mg/kg; oral administration; daily; for 2 weeks; mice) treatment after sensitization with 2,4-dinitrofluorobenzene (DNFB) dampens the degree of the secondary response, with milder infiltration of inflammatory cells into the skin and decreases ratios of interferon-γ⁺ (IFN-γ⁺) cells in a skin contact hypersensitivity model, when compared with vehicle-treated control mice. T_reg depletion before the elicitation of the secondary response abolishes AS2863619-induced suppression. KLRG1⁺ Foxp3⁺ T cells are specifically increased in DNFB sensitized AS2863619-treated mice^[5].

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

405.24

C₁₆H₁₄Cl₂N₈O

2241300-51-4

NC1=NON=C1C(N2C3=CC=C4N=C(C)NC4=C3)=NC5=C2C=CN=C5.[H]Cl.[H]Cl

Room temperature in continental US; may vary elsewhere.

Please store the product under the recommended conditions in the Certificate of Analysis.

• [1]. Fang K, et al. Progress and Future Perspectives of Treg Cell Therapy. Front Biosci (Landmark Ed). 2025;30(11):41250.

  [2]. He H, et al. AS2863619 boosts osteogenesis in periodontal ligament stem cells and mitigates inflammatory impairment. Int Immunopharmacol. 2025;161:115101.  [Content Brief]

  [3]. Bulygin A, et al. Assessment and Characterization of Induced Alloantigen-Specific Regulatory T Cells Obtained by the Inhibition of CDK8/19 with the AS2863619 Compound. Int J Mol Sci. 2025;26(22):10957. Published 2025 Nov 12.

  [4]. Schlotfeldt M, et al. CDK7, CDK9, or CDK11 Inhibition Reduces Neutrophil-Driven Inflammation and Tissue Damage in Experimental Autoimmune Models[J]. bioRxiv, 2025: 2025.11. 19.689221.

  [5]. Akamatsu M, et al. Conversion of antigen-specific effector/memory T cells into Foxp3-expressing Treg cells by inhibition of CDK8/19. Sci Immunol. 2019 Oct 25;4(40). pii: eaaw2707.  [Content Brief]