STAT3 Inhibitor

SC99 is an orally active, selective STAT3 inhibitor targeting JAK2-STAT3 pathway. SC99 docks into the ATP-binding pocket of JAK2. SC99 inhibits phosphorylation of JAK2 and STAT3 with no effects on the other kinases associated with STAT3 signaling. SC99 inhibits platelet activation, aggregation and displays potent anti-myeloma, anti-thrombotic activities.

PROTAC EGFR degrader 14 is a EGFR PROTAC degrader, with a DC₅₀ of 2.9 nM against EGFR^{L858R/T790M/C797S}. PROTAC EGFR degrader 14 forms a stable ternary complex by bridging the ATP-binding pocket of the target protein EGFR with VHL E3 ubiquitin ligase, induces efficient and specific degradation of EGFR mutants via the ubiquitin-proteasome system, and ultimately induces cell cycle arrest and apoptosis. PROTAC EGFR degrader 14 can be used in studies related to non-small cell lung cancer carrying the EGFR^C797S drug-resistant mutation.

STAT3-IN-48 is a Sorafenib analogue and potently inhibits the phosphorylation of STAT3. STAT3-IN-48 induces cell apoptosis through SHP-1 dependent STAT3 inactivation. STAT3-IN-48 does not inhibit kinase activity and has anticancer effects.

Physalin B is an orally active anti-inflammatory and anticancer agent. Physalin B can be isolated from Physalis alkekengi L. var. Franchetii. Physalin B inhibits the activation of the NF-κB, NLRP3 inflammasome, STAT3, PI3K/Akt and Hedgehog signaling pathways, regulates the phosphorylation levels of GSK-3β, p38 MAPK, ERK1/2 and JNK, and promotes the nuclear translocation of NRF2. Physalin B reduces the levels of pro-inflammatory cytokines and factors, induces mitochondrial reactive oxygen species (mito-ROS) production, Apoptosis, G2/M cell cycle arrest and incomplete Autophagy, alters cytoskeleton structure and alleviates oxidative stress. Physalin B reduces cancer cell viability, ameliorates liver and lung tissue damage and alleviates liver fibrosis. Physalin B can be used in research related to ulcerative colitis, breast cancer, acute lung injury, colon cancer, non-alcoholic steatohepatitis, liver fibrosis, lung cancer, pancreatic cancer, lymphoma, ovarian cancer, sarcoma and leukemia.

STAT3-IN-17 is a moderate STAT3 inhibitor (IC₅₀=0.7 μM; HEK-Blue IL-6), with antiproliferative activity in HeLa cells. STAT3-IN-17 has good pharmacokinetic characteristics. STAT3-IN-17 also inhibits pyruvate-ferredoxin oxidoreductase (PFOR), and inhibits Helicobacter pylori.

Patiromer is an orally active, selective and non-absorbable intestinal potassium (K⁺) polymer binder that reversibly binds potassium ions in exchange for calcium (Ca²⁺). Patiromer can rapidly and continuously reduce serum potassium levels, maintain a normal blood potassium state, and reduce serum aldosterone levels. Patiromer also increases fecal potassium excretion. Patiromer is mainly used in the study of hyperkalemia associated with diseases such as chronic kidney disease, diabetes, and heart failure, and is particularly suitable for improving renin-angiotensin-aldosterone system inhibitor (RAASi) therapy.

BP79 is a potent TSLP receptor inhibitor. BP79 disrupts TSLP-mediated ternary complex formation, blocks TSLPR-IL7Rα co-localization, binds and stabilizes TSLPR, and inhibits phosphorylated STAT3/6. BP79 suppresses immune cell infiltration, secretion of IL-13, IL-4. BP79 can be used for the research of inflammation diseases, such as atopic dermatitis, allergic asthma, and allergic rhinitis.

ER-464195-01 is an orally active calreticulin (CRT) and integrin α subunits (ITGAs) binding inhibitor. ER-464195-01 inhibits leukocyte infiltration and subsequent inflammatory cascade reactions by dissociating the binding between CRT and ITGA. ER-464195-01 down-regulates the expression of pro-inflammatory genes (such as TNF-α, IL-1β, IL-6, IL-17f) induced by DSS (HY-116282C), and inhibit the phosphorylation of STAT3 and the production of serum amyloid A (SAA). ER-464195-01 can be used for the study of inflammatory bowel disease (IBD).

PROTAC JAK1/2 degrader-1 is an orally active JAK1/JAK2 PROTAC degrader, with DC₅₀ values of 1.4 μM and 0.92 μM against JAK1 and JAK2, respectively. PROTAC JAK1/2 degrader-1 triggers degradation via a CRBN- and proteasome-dependent pathway. PROTAC JAK1/2 degrader-1 inhibits the secretion of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6). PROTAC JAK1/2 degrader-1 alleviates inflammatory responses and colon injury by inhibiting the JAK/STAT3 signaling pathway. PROTAC JAK1/2 degrader-1 can be used for the research of inflammatory bowel disease.

Tofacitinib (Standard) (Tasocitinib (Standard); CP-690550 (Standard)) is the analytical standard of Tofacitinib (HY-40354). This product is intended for research and analytical applications. Tofacitinib (Tasocitinib) is an orally active, blood-brain barrier permeable selective inhibitor of JAK1/JAK3. Tofacitinib blocks the JAK-STAT/NF-κB signaling pathway, inhibits cytokine signal transduction, phosphorylation of STAT1/STAT5, and suppresses innate and adaptive immune responses. Tofacitinib can be used in research related to major depressive disorder, rheumatoid arthritis, pulmonary diseases, systemic lupus erythematosus, and immune-mediated liver injury.

Azaleatin is an orally active inhibitor of hQC, NS2B-NS3 protease and E. coli β-glucuronidase, with IC₅₀ values of 1.1 μM, 38.00 μg/mL and 0.57 μM, respectively. Azaleatin inhibits the activities of NF-κB, MyD88, JAK1, TLR4, STAT3, IL-1β, IL-6, COX-2, TNF-α and β-glucuronidase, blocks pro-inflammatory signaling pathways, reduces the levels of ROS, MDA and uric acid, elevates the levels of GPx, GSR, GST, SOD, CAT, HO-1 and GSH, scavenges free radicals and exerts reducing capacity. Azaleatin inhibits the expression of pro-apoptotic proteins Bax, Caspase-9 and Caspase-3, and upregulates the expression of anti-apoptotic protein Bcl-2. Azaleatin reduces the levels of cardiac injury markers, restores cardiac histological structure, inhibits Aβ aggregation, dengue protease activity, hepatic stellate cell proliferation and cancer cell growth, and also exhibits antibacterial activity. Azaleatin can be used in studies related to subchronic cardiotoxicity, Alzheimer's disease, dengue fever, hyperuricemia, liver fibrosis, gastric cancer and bacterial infections.

MNK8 is a potent STAT3 (signal transducer and activator of transcription 3) inhibitor. MNK8 inhibits STAT3 activation and reduced its DNA binding ability. MNK8 shows good growth inhibition against hepatocellular carcinoma (HCC) cells. MNK8 induces apoptosis in HCC cells. MNK8 reduces prosurvival proteins expression and migration/invasion of HCC cells.

S3I-1757 is a STAT3 inhibitor. S3I-1757 inhibits the phosphorylation and dimerization of STAT3. S3I-1757 can be used for the research of STAT3 hyperactive cancers such as melanoma.

MMPP is an orally active inhibitor of STAT3 and VEGFR2, as well as an activator of PPARγ. MMPP blocks the VEGFR2/AKT/ERK/NF-κB signaling pathway to inhibit angiogenesis. MMPP inhibits ferroptosis and inflammation, and alleviates sepsis-induced myocardial injury. MMPP induces G1-phase cell cycle arrest and apoptosis, and inhibits the growth of non-small cell lung cancer (NSCLC) and solid tumors. MMPP promotes adipogenesis and glucose uptake. MMPP can be used in research related to NSCLC, type 2 diabetes and myocardial injury.

WB518 is a potent STAT3 inhibitor. WB518 effectively inhibits STAT3 activation and Keratin 17 expression. WB518 effectively alleviates imiquimod (HY-B0180) and TPA (HY-18739)-induced animal psoriasis by inhibiting STAT3 phosphorylation and Keratin 17.

APTSTAT3-9R, a specific STAT3-binding peptide, inhibits STAT3 activation and downstream signaling by specifically blocking STAT3 phosphorylation. APTSTAT3-9R exerts antiproliferative effects and antitumor activity.

Tofacitinib-d₃ citrate (Tasocitinib-d₃ citrate; CP-690550-d₃ citrate) is the deuterated-labeled Tofacitinib citrate (HY-40354A). Tofacitinib citrate (Tasocitinib citrate) is an orally active, blood-brain barrier permeable selective inhibitor of JAK1/JAK3. Tofacitinib citrate blocks the JAK-STAT/NF-κB signaling pathway, inhibits cytokine signal transduction, phosphorylation of STAT1/STAT5, and suppresses innate and adaptive immune responses. Tofacitinib citrate can be used in research related to major depressive disorder, rheumatoid arthritis, pulmonary diseases, systemic lupus erythematosus, and immune-mediated liver injury.

Sorafenib-¹³C,d₃ (Bay 43-9006-¹³C,d₃) is the ¹³C, deuterated-labeled Sorafenib (HY-10201). 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.

1-Stearoyl-sn-glycero-3-phosphocholine-d₃₅ is deuterium labeled 1-Stearoyl-sn-glycero-3-phosphocholine (HY-125771). 1-Stearoyl-sn-glycero-3-phosphocholine is a lysophosphatidylcholine that inhibits HDAC3 activity and phosphorylation of STAT3 in K562 cells. 1-Stearoyl-sn-glycero-3-phosphocholine induces apoptosis and exhibits anticancer activity in chronic myelogenous leukemia (CML) K562 cells.

ENMD-1198 (IRC-110160), an orally active microtubule destabilizing agent, is a 2-methoxyestradiol analogue with antiproliferative and antiangiogenic activity. ENMD-1198 is suitable for inhibiting HIF-1alpha and STAT3 in human HCC cells and leads to reduced tumor growth and vascularization.