stat-3-in-3

STAT3-IN-3 is a potent and selective inhibitor of signal transducer and activator of transcription 3 (STAT3).

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.

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.

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 (GDP) sodium is a nucleoside diphosphate known for activating the adenosine 5'-triphosphate-sensitive K+ channel, serving as a potential iron mobilizer by inhibiting the hepcidin-ferroportin interaction, and modulating the interleukin-6 (IL-6) stat-3 pathway. It is utilized in research on inflammation-related conditions, including anemia of inflammation (AI).

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.

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.