stat-3-in-3

STAT3-IN-3 is a potent and highly selective targeted STAT3 inhibitor with significant anti-proliferative activity. It effectively induces apoptosis in breast cancer cells. As a mitochondrially targeted STAT3 inhibitor with great research potential, it has good application value in tumor mechanism exploration and anti-cancer research.

STAT3-IN-31 (compound K2071), derived from STATtic, acts as an inhibitor of both STAT3 and mitotic processes. This compound interrupts mitotic progression and impacts the formation of the mitotic spindle. Additionally, STAT3-IN-31 hampers migration in glioblastoma cells, suppresses cellular proliferation within tumor spheroids, induces senescence in glioblastoma, and inhibits the growth of Temozolomide-resistant cells while reducing the secretion of the pro-inflammatory cytokine monocyte chemoattractant protein (MCP-1).

STAT3-IN-34 (Compound 15E) acts as a STAT3 inhibitor, blocking both the nuclear translocation and the transcriptional regulator activity of STAT3. It effectively inhibits HaCaT cell proliferation with an IC50 value of 0.008 μM. Additionally, STAT3-IN-34 reduces IL-17A expression and mitigates Imiquimod-induced psoriasis in mouse models.

STAT3-IN-35 is a STAT3 inhibitor that binds to the SH2 domain. This compound inhibits the phosphorylation of STAT3 and exhibits antiproliferative activity in triple-negative breast cancer (TNBC) cell lines. Additionally, STAT3-IN-35 has demonstrated toxicity and potent antitumor activity in TNBC xenograft models.

STAT3-IN-36 (compound 11g) is a tritarget inhibitor that selectively targets LRPPRC, STAT3, and CDK1, exhibiting potent anticancer activity. This compound binds to LRPPRC, STAT3, and CDK1, demonstrating more effective anticancer effects than those of TMF or Capecitabine. Additionally, STAT3-IN-36 exhibits an IC50 value of 1.8 μM in HGC27 cells.

STAT3-IN-39 (compound 10K) is an orally active inhibitor of STAT3, demonstrating effective inhibition of STAT3 phosphorylation with an IC50 of 0.47 μM in NIH-3T3 cells. It hinders TGF-β1-induced fibrotic responses and prevents epithelial-mesenchymal transition in A549 cells. STAT3-IN-39 is applicable for research related to idiopathic pulmonary fibrosis.

STAT3-IN-38 (Compound 4m) is a STAT3 inhibitor with a dissociation constant (K_D) of 45.33 µM for rhSTAT3, and is a derivative of Celastrol. It binds to the SH2 domain of the STAT3 protein, inhibiting phosphorylation at the pTyr705 site and suppressing downstream gene expression of Survivin and Mcl-1. STAT3-IN-38 can arrest the cell cycle and induce apoptosis in colorectal cancer cells.

STAT3-IN-37 (Compound 101) is an inhibitor of STAT3, with an IC50 of 15 nM as measured by DNA-HTRF assay and 2 nM as determined through human whole blood SOCS3 qPCR assay.

STAT3-IN-33 (compound 7f) is a potent STAT3 inhibitor with anticancer properties. It exhibits antiproliferative activity in HCT116, MCF-7, and MDA-MB-231 cells, with IC50 values of 6.44, 3.29, and 4.86 μM, respectively. STAT3-IN-33 is applicable for breast and colon cancer research.

STAT3-IN-B9 (B9) is an inhibitor of abnormal STAT3 activation and inhibits the proliferation of tumor cells including MDA-MB-468, MDA-MB-231, and DU145.

Artesunate (WR-256283) is a semisynthetic derivative of artemisinin and an inhibitor of STAT-3/EXP1. Water-soluble yet relatively unstable in neutral or acidic aqueous solutions, Artesunate is primarily employed for the treatment of malaria.

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.

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).

NF-κB-IN-19 (Compound 8) is an NF-κB inhibitor. It effectively induces DNA damage in tumor cells through the NF-κB signaling pathway and promotes the production of reactive oxygen species (ROS), as well as induces autophagy and apoptosis. Additionally, NF-κB-IN-19 inhibits levels of VEGF and HIF-1α, exerting antiproliferative effects in tumor cells through the PI3K/AKT and STAT-3 pathways. It is also effective in overcoming cisplatin resistance and exhibits antitumor activity.

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.

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]

WP-1034 is a novel Jak-Stat inhibitor, which is active against AML blasts. WP-1034 effectively inhibited proliferation of OCIM2 cells and fresh AML samples. WP-1034 caused cell cycle arrest of OCIM2 cells in sub-Go phase. WP-1034 induced apoptosis of OCIM2 cells and that induction of apoptosis involved cleavage of caspase 3 and the DNA repair enzyme poly (adenosine diphosphate [ADP]-ribose) polymerase (PARP).

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.

Guanosine 5'-diphosphate sodium is a nucleoside diphosphate involved in various intracellular signaling processes, particularly in G protein–coupled receptor signaling, where it regulates G protein activation through GDP/GTP exchange. It may also indirectly influence ion channel activity, such as ATP-sensitive potassium channels.

Guanosine 5'-diphosphate ditromethamine (GDP ditromethamine) is a nucleoside diphosphate that activates ATP-sensitive K+ channels. It acts as a potential iron mobilizer, inhibiting the interaction between hepcidin and ferroportin, and modulating the IL-6/STAT-3 pathway. This compound finds application in inflammation research, such as studying anemia of inflammation (AI).

c-Met-IN-24 (compound 3g) serves as a dual-target inhibitor for STAT-3 (=4.7 μM) and c-MET (=12.67 μM), exhibiting anticancer properties. It arrests the G2/M cell cycle and induces apoptosis in SNB-75 cells, making it applicable in the research of central nervous system cancers.

Guanosine 5'-diphosphate-13C10 dilithium is a 13C-labeled version of Guanosine 5'-diphosphate. GDP is a nucleoside diphosphate that activates adenosine 5'-triphosphate-sensitive K+ channels. It also functions as a potential iron mobilizing agent, capable of disrupting the hepcidin-ferroportin interaction and modulating the IL-6/STAT-3 pathway. Guanosine 5'-diphosphate is utilized in research related to inflammatory conditions, such as anemia of inflammation (AI).

Guanosine 5'-15N5 diphosphate is the 15N-labeled form of Guanosine 5'-diphosphate. Guanosine 5'-diphosphate (T7210) (GDP) is a nucleoside diphosphate that activates ATP-sensitive K+ channels. Additionally, Guanosine 5'-diphosphate (T7210) acts as a potential iron mobilizer, inhibiting the hepcidin-ferroportin interaction and regulating the IL-6/STAT-3 pathway. It is used in inflammation research, including studies on anemia of inflammation (AI).