STAT3 Inhibitor

PROTAC JAK2 degrader-1 is a JAK2 PROTAC degrader, with a DC₅₀ of 27.35 nM. PROTAC JAK2 degrader-1 induces JAK2 degradation via the ubiquitin-proteasome pathway. PROTAC JAK2 degrader-1 inhibits the JAK2-STAT signaling pathway. PROTAC JAK2 degrader-1 induces G₂/M phase arrest and apoptosis in cancer cells. PROTAC JAK2 degrader-1 exhibits antiproliferative activity against cancer cells. PROTAC JAK2 degrader-1 inhibits recombinant human erythropoietin (rhEPO)-mediated polycythemia and splenomegaly in mice. PROTAC JAK2 degrader-1 can be used for research on myeloproliferative neoplasms, including polycythemia vera.

HAT-SIL-TG-1&AT is a Janus tyrosine kinase (JAK) inhibitor with antitumor effects. HAT-SIL-TG-1&AT is the hypoxia-activated prodrug, witch inhibits JAK-STAT signaling in tumor tissue. And HAT-SIL-TG-1&AT inhibits HEL cells proliferation and downregulated phosphorylated STAT3/5 under hypoxic conditions.

STA-1474 is an orally active and highly selective HSP90 inhibitor, as well as a phosphate prodrug of the HSP90 inhibitor STA-9090 (HY-15205). STA-1474 disrupts the chaperone function of HSP90 and promotes the degradation of client proteins. STA-1474 inhibits the phosphorylation of Met, Akt and STAT3, thereby blocking related signaling pathways. STA-1474 induces apoptosis and inhibits proliferation of osteosarcoma cells, and triggers the up-regulation of HSP70 and HSP90. STA-1474 induces tumor regression and caspase-3 activation in mouse osteosarcoma xenograft models. STA-1474 can be used in the research of osteosarcoma.

STAT3/NF-κB-IN-1 is a potentSTAT3 and NF-κB inhibitor with IC₅₀s of 5.86 (STAT3) and 4.22 μM (NF-κB) in 4T1 cells. STAT3/NF-κB-IN-1 is able to induce apoptosis via its upregulation on key apoptotic regulators; caspases-3/9, Bax and downregulation of Bcl-2. STAT3/NF-κB-IN-1 exerts considerable anticancer activity against breast cancer cell lines and reduces tumor volume in vivo. STAT3/NF-κB-IN-1 can be used for the study of breast cancer.

Apoptosis inducer 55 (Compound 10) is an Apoptosis inducer. Apoptosis inducer 55 induces rapid apoptosis via the intrinsic pathway. Apoptosis inducer 55 potently inhibits several signaling cascades including AKT, ERK1/2, STAT1, STAT3, and S6K. Apoptosis inducer 55 has anti-cancer activity against melanoma.

STAT3-IN-47 is an orally active STAT3 inhibitor. STAT3-IN-47 exhibits broad-spectrum anti-tumor activity against HeLa, HepG2, U87, and LN229 cells. STAT3-IN-47 suppresses STAT3 activation in vitro. STAT3-IN-47 can be used for the study of solid tumors, especially central nervous system (CNS) malignancies and hepatocellular carcinoma.

SH-17 is a STAT3 and HDAC inhibitor, with a K_d of 0.87 μM for STAT3, and IC₅₀ values of 115.2 nM and 9.8 nM for HDAC1 and HDAC6, respectively. SH-17 blocks intracellular ATP production and mitochondrial oxidative phosphorylation, induces cell cycle arrest at the G0/G1 phase, and triggers apoptosis. SH-17 is applicable to colon cancer research.

7-epi-Isogarcinol is a polycyclic polyprenylated acylphloroglucinol (PPAP), with moderate antiproliferative activity. 7-epi-Isogarcinol blocks STAT3 signaling pathway, to induce apoptosis and inhibit cell migration.

Lss-11 is a topoisomerase inhibitor. LSS-11 enhances cell death in cancer cells by inducing apoptosis through increasing the DR5 protein level and PARP1 cleavage. LSS-11 dose-dependently reduces STAT3 phosphorylation, downregulates its target genes MDR1 and MRP1, reduces P-gp protein expressionwithout affecting P-gp transport function. Lss-11 is a chemosensitizer and shows synergistic anticancer effect with Paclitaxel (HY-B0015). Lss-11 can be used for the research of paclitaxel-resistant lung cancer.

STAT3-IN-52 hydrochloride is an orally active STAT3 inhibitor with a K_i value of 2.42 μM. STAT3-IN-52 hydrochloride binds directly and selectively to the pY705 site of STAT3 (K_i = 0.44 μM), thereby impairing its function. STAT3-IN-52 hydrochloride induces apoptosis and triggers anti-tumor responses in vivo. STAT3-IN-52 hydrochloride can be used in breast cancer-related research.

AH-26 is a STAT3 inhibitor. AH-26 stabilizes the STAT3 protein, inhibits STAT3 phosphorylation, induces mitochondria-mediated apoptosis, triggers differentiation of leukemia cells, suppresses cancer cell migration, and arrests the cell cycle at the G1 phase. AH-26 exhibits antitumor activity without toxicity in nude mice. AH-26 can be used in the research of leukemia, ovarian cancer, gastric cancer, and pancreatic cancer.

STAT3-IN-44 is a potent STAT3 inhibitor with IC₅₀s of 1.84 (C6 cells) and 4.81 μM (A549 cells). STAT3-IN-44 inhibits STAT3 phosphorylation, downregulates Bcl-2, and upregulates Caspase-3 to promote late-stage apoptosis. STAT3-IN-44 significantly suppresses tumor cell proliferation and migration. STAT3-IN-44 can be used for the study of cancers such as glioma and lung cancer.

Cernuumolide J (TMJ-105) is an JAK2/STAT3 inhibitor. Cernuumolide J induces G2/M phase arrest and apoptosis in HEL leukemia cells by downregulating the phosphorylation of JAK2, STAT3, and Erk, and activating the phosphorylation of JNK and p38 MAPK. Cernuumolide J inhibits HEL leukemia cell growth in a time- and concentration-dependent manner, with an IC₅₀ value of 1.79 μM. Cernuumolide J can be used for research in the field of anti-cancer therapy.

Atractylenolide II (Standard) is the analytical standard of Atractylenolide II. This product is intended for research and analytical applications. Atractylenolide II (Asterolide) is a sesquiterpenoid compound. Atractylenolide II can induce G1 phase cell cycle arrest and apoptosis in B16 melanoma cells. Atractylenolide II is an orally effective anticancer agent that can exert anti-melanoma effects by inhibiting the STAT3 signaling pathway. In addition, Atractylenolide II has been shown to ameliorate myocardial fibrosis, oxidative stress, and neuroprotective activity.

PROTAC ALK degrader-5 (Compound 17) is an efficient ALK PROTAC degrader, with its inhibitory effects on EML4-ALK and NPM-ALK being 27.4 nM and 116.5 nM respectively. PROTAC ALK degrader-5 exhibits potent anti-proliferative activity against H3122 and Karpas 299. PROTAC ALK degrader-5 effectively inhibits the phosphorylation of ALK and STAT3. PROTAC ALK degrader-5 can be used for the study of ALK-driven malignant tumors, such as human non-small cell lung cancer and anaplastic large cell lymphoma.

Antitumor agent-73 is a Diosgenin (HY-N0177) derivative, which inhibits STAT3 signaling and activates Pdia3/ERp57 exogenously. Antitumor agent-73 shows potent anti-tumor activity against various cancer cell lines, 7.9-341.7-fold stronger than Diosgenin.

Glucocorticoid receptor/IL-6-IN-1 (Compound 35) is a selective dual inhibitor targeting the glucocorticoid receptor (GR) and IL-6 signaling pathway (IC₅₀ values of 120 nM and 59 nM, respectively). Glucocorticoid receptor/IL-6-IN-1 inhibits IL-6-induced JAK/STAT3 phosphorylation, blocking inflammatory cytokine transcription. Glucocorticoid receptor/IL-6-IN-1 is promising for research of inflammatory diseases like rheumatoid arthritis and asthma.

W1307 is a selective STAT3 inhibitor with a K_D value of 1.74 μM. W1307 inhibits STAT3 Tyr705 phosphorylation, disrupts STAT3 dimerization, and suppresses STAT3 transcriptional activity. W1307 downregulates the expression of STAT3 downstream targets c-Myc, Mcl-1 and Bcl-2. W1307 transcriptionally inhibits SREBP1 and CPT2 expression to disrupt lipid homeostasis. W1307 shows potent anti-leukemic activity and synergizes with Cytarabine (Ara-C) (HY-13605) to overcome chemoresistance in acute myeloid leukemia (AML).

NSC-368262 is a STAT3 inhibitor. NSC-368262 selectively alkylates and covalently modifies STAT3 Cys468 at the DNA-binding interface of STAT3, blocks the DNA-binding activity of STAT3, and inhibits the phosphorylation of STAT3. NSC-368262 blocks the accumulation of activated STAT3 in the nucleus of cancer cells, induces PARP cleavage and apoptosis in cells, and inhibits tumor growth in mouse models. NSC-368262 can be used in research related to breast cancer and cervical cancer.

XD2-149 is a ZFP91 PROTAC degrader with DC₅₀ values of 0.08 μM and 0.06 μM, respectively. ZFP91 is a bifunctional nuclear protein with both transcription factor and E3 ubiquitin ligase activities, and is classified as an oncogenic non-canonical NF-κB pathway regulator in tumor and immune regulation. XD2-149 induces proteasome-dependent degradation of the E3 ubiquitin-protein ligase ZFP91. XD2-149 inhibits the STAT3 signaling pathway in pancreatic cancer cells and induces NQO1-dependent cell death independent of ZFP91 degradation. XD2-149 can be used for the research of pancreatic cancer.