stat-3-in-1

VEGFR-2/STAT-3-IN-1 (Compound 9f) is a dual inhibitor targeting VEGFR-2 with an IC50 of 26.3 nM and STAT-3 with an IC50 of 5.63 nM. It suppresses the proliferation of cancer cells PANC1 and PC3, with IC50 values of 0.14 and 0.10 µM, respectively, and induces apoptosis in PC3 cells.

STAT3-IN-1 selective and orally active inhibitor of STAT3(in HT29 and MDA-MB 231 cells, with IC50 values of 1.82 μM and 2.14 μM , respectively), induces tumor apoptosis.

(R)-JAK2/STAT3-IN-10a is the R-isomer of JAK2/STAT3-IN-1.JAK2/STAT3-IN-1 is a GP130 D1 structural domain inhibitor with antitumor activity that inhibits the phosphorylation of JAK2 and STAT3. The KD value of (R)-JAK2/STAT3-IN-1 on GP130 protein is 3.8 μM.

JAK2/STAT3-IN-1 is a GP130 inhibitor with anti-tumor effects and can be used to study inflammation, autoimmunity and cancer.

JAK1/STAT3-IN-1 (compound 4f) functions as an anti-atopic dermatitis (AD) agent by inhibiting the JAK1/STAT3 signaling pathway. It has an IC50 value of 2.17 μM for inhibiting NO production. Additionally, JAK1/STAT3-IN-1 improves skin conditions in AD-like mice by reducing inflammatory infiltration, suppressing the expression of p-JAK1/JAK1 and p-STAT3/STAT3, and alleviating the hyperimmune response induced by MC903 (Calcipotriol).

EGFR/STAT3-IN-1 (Compound 5k) is a dual inhibitor targeting both EGFR and STAT3, with IC50 values of 41 nM and 3.34 nM, respectively. It exhibits antitumor activity.

CAY10784 (STAT3-IN-17) is a STAT3 inhibitor with antiproliferative and antitumor activities. CAY10784 showed antibacterial activity against Clostridium difficile.

STAT3-IN-10 (A11) is an inhibitor of STAT3 that directly binds to STAT3 SH2 domain, inhibits tumor cell growth and induces apoptosis in cancer cells (IC 50 = 5.18 μM) [1].

STAT3-IN-11 is a selective STAT3 inhibitor with inhibitory effects on phosphorylation of the STAT3pTyr705 site and phosphorylation of Survivin.STAT3-IN-11 promotes apoptosis in cancer cells and is a candidate compound for the treatment of cancer.

STAT3-IN-13 is a potent STAT3 inhibitor.STAT3-IN-13 has antiproliferative and anticancer activity and acts by binding to the structural domain of STAT3 SH2.STAT3-IN-13 inhibits the phosphorylation of STAT3 Y705, which induces apoptosis and inhibits tumor cell growth and metastasis.STAT3-IN-13 can be used to study breast cancer and liver cancer. The study of breast cancer and hepatocellular carcinoma.

STAT3-IN-12, a potent STAT3 signaling inhibitor, suppresses IL-6-induced JAK/STAT3 pathway activation. This compound inhibits cancer cell proliferation and migration while inducing apoptosis and cell cycle arrest, making it suitable for hepatocellular carcinoma (HCC) and esophageal cancer research.

STAT3-IN-15, a potent and orally active inhibitor targeting STAT3, effectively combats idiopathic pulmonary fibrosis (IPF) by hindering STAT3 phosphorylation. Additionally, it impedes TGF-β1-induced migration and deformation of epithelial cells and prevents epithelial-mesenchymal transition (EMT), offering a multifaceted approach against IPF.

STAT3-IN-14 is a STAT3 inhibitor and has STAT3 phosphorylation inhibitory activity. STAT3-IN-14 can directly bind to the hinge region of STAT3 .

DualCathepsinL/JAK-IN-1 (Compound A8) serves as a dual inhibitor of Cathepsin L (CTSL) and JAK, exhibiting IC50 values of 0.68 μM for CTSL and 337.1 nM, 5.251 nM, 27.29 nM, and 172.6 nM for JAK1/2/3 and TYK2, respectively. This compound effectively prevents the activation of MAPK, NF-κB, and JAK/STAT signaling pathways, leading to significant anti-inflammatory therapeutic effects. DualCathepsinL/JAK-IN-1 is applicable in research on acute lung injury (ALI).

STAT-3/c-Src-IN-1 (Compound 12d) is a dual inhibitor of STAT-3 (IC50=0.844 μM) and c-Src (IC50=0.268 μM). It effectively disrupts tumor cell proliferation, migration, and angiogenesis pathways. This compound exhibits potent antiproliferative activity against melanoma (SK-MEL-2) and central nervous system cancer (SNB-75) cell lines, with GI50 values of -5.75 μM and -5.63 μM, respectively. It induces apoptosis through cell cycle arrest at the G0/G1 and G2/M phases. STAT-3/c-Src-IN-1 shows promise for research in melanoma and glioblastoma.

Lipid-derived lipoxins are produced at the site of vascular and mucosal inflammation where they down-regulate polymorphonuclear leukocyte recruitment and function. 15(R)-Lipoxin A4 (15(R)-LXA4) is derived from the aspirin-triggered formation of 15(R)-HETE from arachidonic acid. [1] [2] 15(R)-LXA4 inhibits LTB4-induced chemotaxis, adherence, and transmigration of neutrophils with twice the potency of LXA4 demonstrating activity in the nM range.[2] [3] The anti-inflammatory effects of aspirin may be ascribed in part to the ability of 15(R)-LXA4 to regulate leukocyte function.[4] 15(R)-LXA4 is reported to promote resolution of inflammation in LPS-treated stromal cells derived from intermediate-stage diseased supraspinatus tendons as evidenced by increased expression of the STAT-6 pathway target genes, ALOX15 and CD206.[5]

1. Curculigoside (Curculigoside A) can prevent bone loss , improve osteogenesis and inhibit osteoclastogenesis of hAFSCs, suggesting its potential use to regulate hAFSC osteogenic differentiation for treating bone disorders. 2. Curculigoside can promote calcium deposition and increase the levels of ALP and Runx2 in osteoblasts under oxidative stress via anti-oxidative character. 3. Curculigoside possesses potent antioxidant properties against oxidative stress insults. can protect endothelial cells against oxidative injury induced by H2O2, suggesting that this compound may constitute a promising intervention against cardiovascular disorders.

Curculigoside (Standard) is a reference standard for research and analysis in studies involving Curculigoside. 1. Curculigoside (Curculigoside A) can prevent bone loss , improve osteogenesis and inhibit osteoclastogenesis of hAFSCs, suggesting its potential use to regulate hAFSC osteogenic differentiation for treating bone disorders. 2. Curculigoside can promote calcium deposition and increase the levels of ALP and Runx2 in osteoblasts under oxidative stress via anti-oxidative character. 3. Curculigoside possesses potent antioxidant properties against oxidative stress insults. can protect endothelial cells against oxidative injury induced by H2O2, suggesting that this compound may constitute a promising intervention against cardiovascular disorders.

3-O-Methylgallic acid (3,4-Dihydroxy-5-methoxybenzoic acid) reduces cell proliferation in Caco-2 cells (IC50 = 24.1 μM) more effectively than anthocyanins and may offer protection against colon cancer after its formation in the gut. It inhibits transcription factors NF-κB, AP-1, STAT-1, and OCT-1, which are known to be activated in colorectal cancer.