STAT Inhibitor

STAT6-IN-2 (Compound R-84) is a STAT6 inhibitor that can inhibit the tyrosine phosphorylation of STAT6. STAT6-IN-2 can also inhibit the secretion of eotaxin-3. STAT6-IN-2 can be used in the research of immune diseases and allergic inflammatory diseases such as asthma.

OSM-SMI-10B a derivative of OSM-SMI-10. OSM-SMI-10B significantly reduces OSM-induced STAT3 phosphorylation in cancer cells upon co-incubation with OSM (Oncostatin M).

Iruplinalkib (WX-0593) is an orally active and selective ALK/ROS1 inhibitor. Iruplinalkib can effectively inhibit tyrosine autophosphorylation of ALK and mutant ALK, EGFR, with the IC₅₀ between 5.38 and 16.74 nM. Iruplinalkib is also a suppressive agent of the transporter MATE1, MATE2K, P-gp and BCRP. Iruplinalkib can be used in the study of non-small cell lung cancer.

Phellopterin, an orally active furocoumarin with multiple biological activities. Phellopterin is a partial agonist of the central benzodiazepine receptors. Phellopterin exerts anti-inflammatory effects by upregulating SIRT1, downregulating ICAM-1 (reducing chronic inflammation, aiding diabetic ulcer healing), inhibiting STAT3 phosphorylation (easing atopic dermatitis inflammation), regulating Akt/PKC pathways (lowering TNF-α-induced VCAM-1 to block monocyte adhesion), and inhibiting TLR4/NF-κB pathway and macrophage M2 polarization (alleviating colitis-related cancers). Phellopterin suppresses ovarian cancer progression via inhibiting the PU.1/CLEC5A/PI3K-AKT loop (inducing cell cycle arrest, apoptosis, DNA damage). Phellopterin alleviates murine diabetes by promoting adipocyte differentiation and increasing PPARγ. Phellopterin also has anti-HSV-1 activity. Phellopterin can be used for studying anti-inflammation, anti-cancer (e.g., ovarian cancer, colitis cancer), blood glucose lowering, anti-diabetes, and anti-virus.

Cycloguanil (Chlorguanide triazine) hydrochloride is a dihydrofolate reductase (DHFR) inhibitor with an IC₅₀ of 10.8 μM against human DHFR. Cycloguanil hydrochloride blocks the folate metabolic pathway, thereby affecting nucleotide synthesis and interfering with DNA replication. Cycloguanil inhibits DHFR in Plasmodium and is thus used in malaria research. Cycloguanil hydrochloride also potently inhibits DHFR in human cancer cells and blocks the transcriptional activity of STAT3, thereby exhibiting anticancer activity.

Panaxadiol (20(R)-Panaxadiol) is an orally active HIF-1α/STAT3 inhibitor. Panaxadiol can suppress HIF-1α and STAT3 then lead to downregulation of programmed cell death-ligand 1 (PD-L1) expression. Panaxadiol shows anticancer, cardioprotective, anti-arrhythmic, and antioxidative activities.

PM-43I is a potent STAT6 inhibitor and can reduce STAT6 phosphorylation level. PM-43I can be used in allergic lung disease, allergic rhinitis, chronic pulmonary obstructive disease and cancer research^[1].

Atranorin is a secondary metabolite of lichens and AKT inhibitor. Atranorin possesses multiple activities such as antibacterial, anti-inflammatory, antioxidant, anti-glycation, analgesic, and anti-tumor effects. Atranorin has IC₅₀ values for scavenging DPPH and ABTS free radicals of 117 μM and less than 10 μM, respectively. Additionally, Atranorin also exhibits effects in promoting wound healing. Atranorin can be used in the research of various diseases, including myelodysplastic syndromes, tumors, and inflammatory conditions.

GMB-475 is a potent BCR-ABL1 PROTAC based on Von Hippel-Lindau (VHL). GMB-475 targets the nutmeg pocket of ABL1 in an ectopic manner and degrades BCR-ABL1 protein through the ubiquitin proteasome pathway. GMB-475 inhibits the proliferation of human K562 cells and mouse Ba/F3 cells, and is used for the study of chronic myeloid leukemia.

Cenisertib (AS-703569) is an ATP-competitive multi-kinase inhibitor that blocks the activity of Aurora-kinase-A/B, ABL1, AKT, STAT5 and FLT3. Cenisertib induces major growth-inhibitory effects by blocking the activity of several different molecular targets in neoplastic mast cells (MC). Cenisertib inhibits tumor growth in xenograft models of pancreatic, breast, colon, ovarian, and lung tumors and leukemia.

(R)-Lisofylline ((R)-Lisophylline) is a (R)-enantiomer of the metabolite of Pentoxifylline with anti-inflammatory properties. (R)-Lisofylline is a lysophosphatidic acid acyltransferase inhibitor with an IC₅₀ of 0.6 μM and interrupts IL-12 signaling-mediated STAT4 activation. (R)-Lisofylline has the potential for type 1 diabetes, autoimmune disorders research.

Niclosamide (BAY2353) olamine is an orally active antihelminthic agent used in parasitic infection research. Niclosamide olamin is a STAT3 inhibitor with an IC₅₀ of 0.25 μM in HeLa cells. Niclosamide olamin has biological activities against cancer, and inhibits DNA replication in Vero E6 cells.

Sorafenib (Standard) (Bay 43-9006 (Standard)) is the analytical standard of Sorafenib (HY-10201). This product is intended for research and analytical applications. Sorafenib (Bay 43-9006) is a potent oral active multikinase inhibitor. Sorafenib blocks autophosphorylation and activity of receptor tyrosine kinases (VEGFR-2, VEGFR-3) and RAF family kinases, thereby suppressing the RAF/MEK/ERK and PI3K/Akt pathways, inhibiting STAT3 phosphorylation, and selectively inhibiting the MAPK pathway in cancer cells. Sorafenib induces cell cycle arrest, autophagy, apoptosis, and PARP cleavage, reduces Bcl-2, Bcl-XL, cyclin D1 levels, and activates Bak and Bax. Sorafenib inhibits tumor growth and metastasis in mouse and rat models. Sorafenib can be used for cancer research, such as colon, breast, non-small-cell lung cancer (NSCLC), ovarian, pancreatic, melanoma, colorectal and hepatocellular carcinoma.

TL13-112 is a ALK PROTAC degrader. TL13-112 degrades the NPM-ALK protein by recruiting the CRBN E3 ligase, thereby blocking oncogenic signal transduction such as STAT3, ERK and AKT, and relieving the transcriptional repression of CD45, CCR7 and PI3Kδ. TL13-112 can be used in related research on anaplastic large cell lymphoma.

L002 is a potent, cell permeable, reversible and specific acetyltransferase p300 (KAT3B) inhibitor with an IC₅₀ of 1.98 μM. L002 binds the acetyl-CoA pocket and competitively inhibits the FATp300 catalytic domain, blocks histone acetylation and p53 acetylation, and inhibits STAT3 activation. L002 has the potential for hypertension-induced cardiac hypertrophy and fibrogenesis treatment.

S-Propargylcysteine (SPRC), a structural analog of S-allyl cysteine (SAC), is a slow H₂S-releasing compound. S-Propargylcysteine reduces Ca²⁺ accumulation and inflammatory cytokines, inhibits STAT3, and elevates p53 and Bax. S-Propargylcysteine has anti-inflammatory activity and protects mice against acute pancreatitis. S-Propargylcysteine also has cardioprotective, neuroprotective acitivties.

Tetramethylcurcumin (FLLL31), derived from curcumin, specifically suppresses the phosphorylation of STAT3 by binding selectively to Janus kinase 2 and the STAT3 Src homology-2 domain. Tetramethylcurcumin exhibits anti-inflammatory and anti-cancer effects.

(-)-Asarinin is a tetrahydrofurofurano lignan with various biological activities. (-)-Asarinin induces apoptosis in cancer cells. (-)-Asarinin promotes mitochondrial ROS accumulation, inhibits the STAT3 signaling pathway and induces apoptosis in precancerous cells. (-)-Asarinin is a Src family kinase inhibitor that suppresses mast cell activation. (-)-Asarinin is a non-competitive Δ5-desaturase inhibitor with a K_i of 0.28 mM. (-)-Asarinin possesses pain relief, anti-viral, anti-allergic and anti-tuberculous bacilli, and anti-tumor effects.

Calenduloside E is a pentacyclic triterpenoid saponin that can be extracted from the bark and roots of Aralia ovata, and has anti-inflammatory and anti-apoptotic activities. Calenduloside E alleviates atherosclerosis by regulating macrophage polarization, improves mitochondrial function by regulating the AMPK-SIRT3 pathway, and alleviates acute liver injury. In addition, Calenduloside E promotes the interaction between L-type calcium channels and Bcl-2 related apoptosis genes, inhibits calcium overload, and alleviates myocardial ischemia/reperfusion injury. Calenduloside E also improves non-alcoholic fatty liver disease by regulating heat shock-dependent pathways, and inhibits ROS mediated JAK1-STAT3 pathways to reduce cellular inflammatory responses.

inS3-54A18 is a potent STAT3 inhibitor, with anti-cancer properties.