STAT5
STAT5 comprises STAT5A and STAT5B, transcription factors that regulate hematopoietic cell proliferation, differentiation, and apoptosis[1]. Mechanistically, STAT5 tyrosine phosphorylation in peripheral T cells is driven by cytokine receptor signaling rather than the T-cell receptor complex[2]. This cytokine-linked pathway supports immune regulation, lymphocyte development, and cell survival programs[3]. In disease contexts, STAT5B deficiency is associated with growth failure, immunodeficiency, and severe pulmonary disease[4]. Compared with STAT5A, STAT5B shows dominant activity in effector and regulatory T-cell responses, with paralog dose explaining much functional specificity[5]. In BCR/ABL leukemia models, STAT5B, but not STAT5A, serves as the major STAT5 isoform driving leukemogenesis[6]. For experimental applications, AC-4-130 directly binds STAT5 and disrupts activation, dimerization, nuclear translocation, and STAT5-dependent transcription in AML models[7]. Pimozide also decreases survival of chronic myelogenous leukemia cells resistant to kinase inhibitors[8].
References:
- [1]. Nosaka T, et al. STAT5 as a molecular regulator of proliferation, differentiation and apoptosis in hematopoietic cells. EMBO J. 1999 Sep 1;18(17):4754-65. [Content Brief]
- [2]. Moriggl R, et al. Stat5 activation is uniquely associated with cytokine signaling in peripheral T cells. Immunity. 1999 Aug;11(2):225-30. [Content Brief]
- [3]. Smith MR, et al. STAT5b: A master regulator of key biological pathways. Front Immunol. 2023 Jan 23;13:1025373. [Content Brief]
- [4]. Nadeau K, et al. STAT5b deficiency: an unsuspected cause of growth failure, immunodeficiency, and severe pulmonary disease. J Pediatr. 2011 May;158(5):701-8. [Content Brief]
- [5]. Villarino A, et al. Signal transducer and activator of transcription 5 (STAT5) paralog dose governs T cell effector and regulatory functions. Elife. 2016 Mar 21;5:e08384. [Content Brief]
- [6]. Kollmann S, et al. Twins with different personalities: STAT5B-but not STAT5A-has a key role in BCR/ABL-induced leukemia. Leukemia. 2019 Jul;33(7):1583-1597. [Content Brief]
- [7]. Wingelhofer B, et al. Pharmacologic inhibition of STAT5 in acute myeloid leukemia. Leukemia. 2018 May;32(5):1135-1146. [Content Brief]
- [8]. Nelson EA, et al. The STAT5 inhibitor pimozide decreases survival of chronic myelogenous leukemia cells resistant to kinase inhibitors. Blood. 2011 Mar 24;117(12):3421-9. [Content Brief]
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STAT5 Related Products (70)
Related Products (70)
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Antibodies (5)
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WYE-151650
0 ImagesCat. No.: HY-120457CAS No.: 1141855-86-8WYE-151650 is a selective JAK-3 inhibitor. WYE-151650 suppresses IL-2-induced STAT-5 phosphorylation and cell proliferation mediated by JAK-3. WYE-151650 is promising for research of autoimmune diseases.
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PF15
0 ImagesCat. No.: HY-143286CAS No.: 2892631-70-6PF15 is an orally active FLT3-ITD PROTAC degrader with a DC50 of 76.7 nM and an IC50 of 36 nM against FLT3-ITD. PF15 induces FLT3-ITD protein degradation, thereby downregulating its phosphorylation level. PF15 inhibits the proliferation of FLT3-ITD-positive cells and reduces the phosphorylation level of STAT5, a downstream molecule of FLT3-ITD. PF15 exhibits efficacy in in vivo xenograft models of acute myeloid leukemia and prolongs survival. PF15 can be used for the research of acute myeloid leukemia.
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BCR-ABL degrader 1
0 ImagesCat. No.: HY-180798BCR-ABL degrader 1 is a hydrophobic tag degrader with GNF‑2 (HY-11007) as the ligand and Boc2His (HY-185595) as the hydrophobic tag. BCR-ABL degrader 1 mediates the degradation of BCR‑ABL with a DC50 of 19.9 μM. BCR-ABL degrader 1 induces the degradation of BCR-ABL fusion protein via the ubiquitin-proteasome pathway, a process involving Hsp70 and Hsp90. BCR-ABL degrader 1 downregulates p‑STAT5 and p‑SHP2, the downstream signaling molecules of BCR‑ABL. BCR-ABL degrader 1 can be used in the research of chronic myeloid leukemia.
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FLT3-IN-28
0 ImagesCat. No.: HY-170576FLT3-IN-28 (Compound 12y) is an orally active FLT3 inhibitor with antitumor activity. FLT3-IN-28 selectively inhibits cancer cells harboring the FLT3 internal tandem duplication (ITD) mutation, with IC50 values of 85, 290, 130, 65, and 220 nM for BaF3-FLT3-ITD, BaF3-TEL-VEGFR2, MV4-11, MOLM-13, and MOLM-14 cell lines respectively (MV4-11 and MOLM-13/14 are acute myeloid leukemia (AML) cell lines carrying the FLT3-ITD mutation). Additionally, FLT3-IN-28 can downregulate the phosphorylation levels of FLT3 and STAT5 in MOLM-13 cells and induce cell cycle arrest and Apoptosis. FLT3-IN-28 has an oral bioavailability of 19.2% in SD rats and can prolong survival in a dose-dependent manner in NSG mice xenografted with MOLM-13 cells. FLT3-IN-28 holds promise for research in cancer fields related to FLT3-ITD.
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MA191
0 ImagesCat. No.: HY-175273MA191 is a FLT3 PROTAC degrader. MA191 targets and degrades mutant FLT3-ITD protein by recruiting the VHL E3 ligase in a manner dependent on ubiquitination and BIM, thereby blocking aberrant downstream MAPK/STAT5 signaling pathways and inducing apoptosis. MA191 can be used in research related to acute myeloid leukemia.
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JAK2-IN-18
0 ImagesCat. No.: HY-179687CAS No.: 3108318-77-7JAK2-IN-18 (Compound example1) is a selective JAK2 inhibitor. JAK2-IN-18 can inhibit JAK-STAT signaling and shows an IC50 of <100 nM for pSTAT5 in HEL9217 cells. JAK2-IN-18 can inhibit the proliferation of abnormally proliferating myeloid cells and can be used for the research of myeloproliferative disorders, such as essential thrombocythemia.
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LWY713
0 ImagesCat. No.: HY-157213LWY713 is a FLT3 PROTAC degrader with a DC50 of 0.64 nM. LWY713 selectively induces FLT3 degradation in a cereblon- and proteasome-dependent manner. LWY713 induces G0/G1 cell cycle arrest and triggers apoptosis. LWY713 upregulates PARP and cleaved caspase 3, and inhibits the phosphorylation of FLT3, STAT5, AKT and Erk. LWY713 exhibits antitumor activity in xenograft mouse models. LWY713 can be used for the research of acute myeloid leukemia.
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JAK2-IN-13
0 ImagesCat. No.: HY-174988JAK2-IN-13 is a potent and orally active JAK2 inhibitor with an IC50 of 54.7 nM. JAK2-IN-13 downregulates the expressions of p-STAT3 and p-STAT5. JAK2-IN-13 exhibits good bioavailability and potent inhibition of rhEPO-induced extramedullary erythropoiesis and polycythemia vera. JAK2-IN-13 can be used for the study of myeloproliferative neoplasms.
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PROTAC JAK2 degrader-1
0 ImagesCat. No.: HY-174428PROTAC 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.
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HAT-SIL-TG-1&AT
0 ImagesCat. No.: HY-149257CAS No.: 2973282-50-5HAT-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.
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FLT3-IN-41
0 ImagesCat. No.: HY-182281FLT3-IN-41 is a highly potent FLT3 inhibitor. The IC50 values of FLT3-IN-41 against human FLT3-ITD and FLT3-WT are 3.16 nM and 294.7 nM, respectively. By binding to the ATP-binding pockets of FLT3-ITD and FLT3-WT and forming hydrogen bonds with hinge region residues and Phe830, FLT3-IN-41 inhibits the STAT5, Akt and Erk signaling pathways. FLT3-IN-41 induces G2/M phase arrest and promotes apoptosis in FLT3-ITD-positive acute myeloid leukemia cells, exhibiting significant antiproliferative activity. FLT3-IN-41 serves as a valuable tool for the study of acute myeloid leukemia.
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AK305
0 ImagesCat. No.: HY-184991CAS No.: 2982853-56-3AK305 is a small-molecule ligand for the SH2 domains of STAT5A, STAT5B and STAT6, with a Ki of 0.4 μM for STAT6 and a Ki of 1.0 μM for both STAT5A and STAT5B. AK305 exhibits only very low or no cell growth inhibitory activity in leukemia cells and does not alter STAT protein levels. AK305 serves as the STAT5 ligand for AK-2292 (HY-148813), a STAT5 PROTAC degrader. AK305 can be used in the research of acute myeloid leukemia.
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NVP-BVB808
0 ImagesCat. No.: HY-182430CAS No.: 1180158-99-9NVP-BVB808 is a selective and ATP-competitive JAK2 inhibitor with an IC50 of 0.35 nM. NVP-BVB808 binds to JAK2’s ATP-binding site, stabilizes JAK2’s active conformation, increases JAK2 activation loop phosphorylation, and blocks downstream kinase function. NVP-BVB808 exhibits antiproliferative and pro-apoptosis effects, suppresses constitutive STAT5a phosphorylation. NVP-BVB808 can be used for the research of cancer, such as leukemia.
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PD-305
0 ImagesCat. No.: HY-183937APD-305 is a selective PTPN2 PROTAC degrader, with DC50 values of 0.25 nM and 5.11 nM against PTPN2 and PTPN1, respectively. PD-305 enhances IFN-γ-induced STAT1 phosphorylation, inhibits the proliferation of IFN-γ-stimulated colorectal cancer cells, promotes CD8+ T cell activation, enhances the tumor-killing activity of T cells, and suppresses tumor growth in mouse models. PD-305 can be used for the research of colorectal cancer.
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JAK2-IN-9
0 ImagesCat. No.: HY-155746CAS No.: 2568842-26-0JAK2-IN-9 is an orally active selective JAK2 inhibitor with a human IC50 of 5 nM. JAK2-IN-9 inhibits JAK2 kinase activity, blocks JAK2 phosphorylation, and suppresses the activation of the downstream JAK2-STAT signaling pathway. JAK2-IN-9 inhibits the phosphorylation of STAT3, STAT5 and AKT in cancer cells. JAK2-IN-9 induces cancer cell apoptosis (apoptosis) and cell cycle arrest. JAK2-IN-9 can be used for the research of myeloproliferative neoplasms.
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VS1150
0 ImagesCat. No.: HY-176269CAS No.: 2855238-97-8VS1150 (Compound 11) is a BCR-ABL-targeting phosphorylation-inducing chimeric small molecule (PHICS). VS1150 significantly inhibits oncogenic kinase BCR-ABL signaling by inducing inhibitory phosphorylation at its Y253 (EC50: 69 nM), subsequently triggering cell apoptosis. VS1150 also inhibits other oncogenic ABL fusions and drug-resistant mutants like T315I. VS1150 can be used for chronic myeloid leukemia (CML) and other ABL fusion-driven cancers research.
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FLT3-IN-32 hydrochloride
0 ImagesCat. No.: HY-174437BCAS No.: 3047195-66-1FLT3-IN-32 hydrochloride is a potent and orally active FLT3 inhibitor with an IC50s of 0.29 nM, 0.77 nM and 2.07 nM against FLT3-ITD, FLT3-D835Y and FLT-N676K. FLT3-IN-32 hydrochloride reduces the phosphorylation of FLT3 and its downstream signaling molecules (STAT5, MAPK, AKT) to induce FLT3-mutated Ba/F3 cells apoptosis. FLT3-IN-32 hydrochloride shows significant anti-tumor efficacy in n the MV4-11 xenograft model. FLT3-IN-32 hydrochloride can be used for the study of acute myeloid leukemia (AML).
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Tyk2-IN-22-d3
0 ImagesCat. No.: HY-169984SCAS No.: 1771691-32-7Tyk2-IN-22-d3 (Compound 1) is the deuterated analog of Tyk2-IN-22 (HY-168339). Tyk2-IN-22 (Compound A8) is a selective inhibitor for tyrosine kinase 2 (Tyk2), that it inhibits Tyk2, JAK1, and JAK3 with IC50s of 9.7, 148.6, and 883.3 nM, respectively. Tyk2-IN-22 inhibits the downstream STAT5 phosphorylation.
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JAK2-IN-21
0 ImagesCat. No.: HY-183670CAS No.: 3038340-43-8JAK2-IN-21 is a Janus kinase 2 (JAK2) inhibitor with an IC50 of 12.25 nM. JAK2-IN-21 inhibits the JAK2/STAT3/STAT5 tumor-promoting signaling pathway and reduces JAK2 protein expression. JAK2-IN-21 exhibits selective cytotoxicity against HPV-positive cancer cells and induces cancer cell apoptosis. JAK2-IN-21 can be used in the research of HPV-positive cervical cancer.
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JAK2-IN-14
0 ImagesCat. No.: HY-175684CAS No.: 3087335-24-5JAK2-IN-14 is an orally active JAK2 inhibitor with an IC50 of 2 nM. JAK2-IN-14 demonstrates 89.5-, 80.5-, and 51-fold selectivity over JAK1, JAK3, and TYK2, respectively. JAK2-IN-14 inhibits STAT5 signaling pathway. JAK2-IN-14 causes tumor cell cycle arrest and apoptosis. JAK2-IN-14 can used for the study of myeloproliferative neoplasms (MPNs).
