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phosphorylation of STAT5

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Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-107429
    Abrocitinib
    Maximum Cited Publications
    11 Publications Verification

    PF-04965842

    		 JAK Inflammation/Immunology
    Abrocitinib (PF-04965842) is a potent, orally active and selective JAK1 inhibitor, with IC50s of 29 and 803 nM for JAK1 and JAK2, respectively. Abrocitinib (PF-04965842) exhibits less active effect on TYK2 (IC50, 1.253 μM), and inhibits phosphorylation of STAT1, STAT3 and STAT5 after stimulation. Effective in autoimmune disease .
    Abrocitinib
  • HY-148748
    Butyzamide
    3 Publications Verification

    		 JAK STAT p38 MAPK Cardiovascular Disease
    Butyzamide is an orally active activator of Mpl, a thrombopoietin (TPO) receptor. Butyzamide increases the phosphorylation level of JAK2, STAT3, STAT5 and MAPK. Butyzamide increases the level of platelets in mouse xenotransplantation assay .
    Butyzamide
  • HY-126370A
    Geranylgeranyl pyrophosphate triammonium

    		Endogenous Metabolite YAP Apoptosis Interleukin Related STAT ERK Ras Cancer
    Geranylgeranyl pyrophosphate triammonium is a type of isoprenoid metabolic intermediate, mainly synthesized through the mevalonate pathway. Geranylgeranyl pyrophosphate triammonium is a key precursor in various biological synthesis processes, especially as a necessary substrate for post-translational modification of proteins - geranylgeranyl phosphorylation. Geranylgeranyl pyrophosphate triammonium regulates various cellular processes and disease progression through protein geranylgeranyl phosphorylation, such as activating the YAP signaling pathway, promoting cell proliferation and inhibiting apoptosis; promoting IL-2 production and STAT5 phosphorylation; and influencing metabolic homeostasis and cancer, etc .
    Geranylgeranyl pyrophosphate triammonium
  • HY-N0366
    Sennoside B
    3 Publications Verification

    		 PDGFR Inflammation/Immunology
    Sennoside B is a potent and orally active platelet-derived growth factor (PDGF) inhibitor. Sennoside B inhibits cell proliferation and the expression of phosphorylation of PDGFR-β, STAT-5, AKT and ERK induced by PDGF-BB. Sennoside B shows gastroprotective activities. Sennoside B has the potential for the research of gastritis .
    Sennoside B
  • HY-13775
    XL019
    5 Publications Verification

    		 JAK Apoptosis Cancer
    XL019?is a potent, orally active, and selective JAK2 inhibitor, with IC50s of 2.2, 134.3, and 214.2 nM for JAK2, JAK1 and JAK3, respectively. XL019 shows 50-fold or greater selectivity for JAK2, versus a panel of over 100 serine/threonine and tyrosine kinases, including other members of the JAK family. XL019 potently inhibits STAT3 and STAT5 phosphorylation in cells harboring either JAK2V617F or wild-type JAK2 .
    XL019
  • HY-111388A
    Romaciclib monohydrochloride
    5+ Cited Publications

    SEL120-34A monohydrochloride

    		 CDK Cancer
    SEL120-34A monohydrochloride is an ATP-competitive and selective CDK8 inhibitor, inhibits kinase activities of CDK8/CycC and CDK19/CycC complexes with IC50s of 4.4 nM and 10.4 nM, respectively, with a Kd of 3 nM for CDK8. SEL120-34A monohydrochloride weakly inhibits CDK9 (calculated IC50=1070 nM), but shows no obvious activity against CDK1, 2, 4, 6, 5, 7. SEL120-34A monohydrochloride inhibits phosphorylation of STAT1 S727 and STAT5 S726 . Has anti-tumor activity .
    Romaciclib monohydrochloride
  • HY-12960
    SKLB4771

    FLT3-​IN-​1

    		 FLT3 c-Kit Apoptosis Cancer
    SKLB4771 is a potent and selective Flt3 inhibitor with an IC50 value of 10 nM. SKLB4771 downregulates the phosphorylation of FLT3/STAT5/ERK, blocks cell proliferation, and induces apoptosis in tumor tissue .
    SKLB4771
  • HY-13905
    Flumatinib mesylate
    3 Publications Verification

    HHGV678 mesylate

    		 Bcr-Abl c-Kit PDGFR Cancer
    Flumatinib (HHGV678) mesylate is an orally active and selective inhibitor of Bcr-Abl. Flumatinib mesylate inhibits c-Abl, PDGFRβ and c-Kit with IC50 values of 1.2, 307.6 and 665.5 nM, respectively. Flumatinib mesylate inhibits Bcr-Abl autophosphorylation and Stat5 and Erk1/2 phosphorylation. Flumatinib mesylate inhibits tumor growth in chronic myelogenous leukemia model .
    Flumatinib mesylate
  • HY-126370
    Geranylgeranyl pyrophosphate

    		Endogenous Metabolite YAP Apoptosis Interleukin Related STAT ERK Ras Cancer
    Geranylgeranyl pyrophosphate is a type of isoprenoid metabolic intermediate, mainly synthesized through the mevalonate pathway. Geranylgeranyl pyrophosphate is a key precursor in various biological synthesis processes, especially as a necessary substrate for post-translational modification of proteins - geranylgeranyl phosphorylation. Geranylgeranyl pyrophosphate regulates various cellular processes and disease progression through protein geranylgeranyl phosphorylation, such as activating the YAP signaling pathway, promoting cell proliferation and inhibiting apoptosis; promoting IL-2 production and STAT5 phosphorylation; and influencing metabolic homeostasis and cancer, etc .
    Geranylgeranyl pyrophosphate
  • HY-P991424
    GSK2618960

    		Interleukin Related STAT Inflammation/Immunology
    GSK2618960 is a human monoclonal antibody (mAb) targeting IL-7Ra/CD127. GSK2618960 inhibits IL-7-induced STAT5 phosphorylation. GSK2618960 enhances CD4 T cell proliferation response and increases CD83, CD86, and CD209 expression in PBMCs. GSK2618960 can be used for the research of autoimmune and allergic inflammatory diseases. Recommended isotype control: Human IgG1 kappa, Isotype Control (HY-P99001) .
    GSK2618960
  • HY-P10283
    S1H

    		GHSR STAT Endocrinology
    S1H, a mimetic of hGH, is a human growth hormone receptor (hGHR) antagonist. S1H inhibits the interaction of hGH with hGHR. S1H inhibits phosphorylation of STAT5 in cells co-treated with hGH .
    S1H
  • HY-P991358
    XOMA-213

    LFA-102; X213

    		 Estrogen Receptor/ERR STAT Akt Cancer
    XOMA-213 (LFA-102; X213) is a human monoclonal antibody (mAb) targeting the prolactin receptor (PRLR), with a Kd value of 2 nM against the human target. XOMA-213 blocks PRL-induced cell proliferation and inhibits the activation of multiple PRLR ligands, including PRL and human growth hormone (hGH). XOMA-213 suppresses PRL-induced phosphorylation of Stat5, Akt and ERK1/2 in cells. XOMA-213 induces tumor regression, delays disease progression, and inhibits PRLR signaling as well as tumor growth. XOMA-213 can be used in research related to breast cancer .
    XOMA-213
  • HY-148748G
    Butyzamide

    		JAK STAT p38 MAPK Cardiovascular Disease
    Butyzamide (GMP) is Butyzamide (HY-148748) produced by using GMP guidelines. GMP small molecules works appropriately as an auxiliary reagent for cell therapy manufacture. Butyzamide is an orally active activator of Mpl, a thrombopoietin (TPO) receptor. Butyzamide increases the phosphorylation level of JAK2, STAT3, STAT5 and MAPK. Butyzamide increases the level of platelets in mouse xenotransplantation assay .
    Butyzamide
  • HY-107429R
    Abrocitinib (Standard)

    PF-04965842 (Standard)

    		 Reference Standards JAK Inflammation/Immunology
    Abrocitinib (Standard) is the analytical standard of Abrocitinib. This product is intended for research and analytical applications. Abrocitinib (PF-04965842) is a potent, orally active and selective JAK1 inhibitor, with IC50s of 29 and 803 nM for JAK1 and JAK2, respectively. Abrocitinib (PF-04965842) exhibits less active effect on TYK2 (IC50, 1.253 μM), and inhibits phosphorylation of STAT1, STAT3 and STAT5 after stimulation. Effective in autoimmune disease .
    Abrocitinib (Standard)
  • HY-167692
    JI069

    		STAT Others
    JI069 is a novel JAK-STAT inhibitor that demonstrates potent activity in suppressing Th1, Th2, and Th17 differentiation while promoting iTreg differentiation. JI069 effectively inhibits STAT3 activation as well as the activation of other STATs, including STAT1, STAT5, and STAT6. JI069 has shown significant therapeutic potential in alleviating symptoms of collagen-induced arthritis in mice while inhibiting cytokine production from T cells and the phosphorylation of STAT3 in synovial cells.
    JI069
  • HY-155746
    JAK2-IN-9

    		JAK Infection Inflammation/Immunology
    JAK2-IN-9 (Compound A8) is a selective JAK2 inhibitor (IC50: 5 nM). JAK2-IN-9 inhibits the phosphorylation of JAK2, STAT3, and STAT5. JAK2-IN-9 has metabolic stabilities. JAK2-IN-9 induces apoptosis. JAK2-IN-9 can be used for research of myeloproliferative neoplasms (MPNs) .
    JAK2-IN-9
  • HY-143286A
    PF15 TFA

    		PROTACs FLT3 Cancer
    PF15 TFA is a PROTAC connected by ligands for FLT3 kinase and CRBN. PF15 TFA is a high selective FLT3-ITD degrader, with a DC50 of 76.7 nM. PF15 TFA significantly inhibits the proliferation of FLT3-ITD-positive cells, down-regulates the phosphorylation of FLT3 and STAT5. PF15 TFA also inhibits tumor growth in mouse models and can be used in study of leukemia .
    PF15 TFA
  • HY-170837
    STAT5-IN-3

    		STAT Cancer
    STAT5-IN-3 (Compound 14a) is a STAT5 inhibitor with anticancer activity. STAT5-IN-3 blocks the tyrosine phosphorylation of STAT5A/5B at the Y694/699 sites and significantly reduces the expression of STAT5B protein, thereby inhibiting downstream gene transcription and blocking the proliferation and survival of leukemia cells. Additionally, STAT5-IN-3 holds significant value in overcoming chemotherapy resistance .
    STAT5-IN-3
  • HY-125151
    BP-1-108

    		STAT Apoptosis Cancer
    BP-1-108 is a selective inhibitor of STAT5 (Ki=8.3 μM) with anticancer activity. BP-1-108 induces apoptosis of leukemia cells by inhibiting the phosphorylation of STAT5. BP-1-108 can be used in the study of acute myeloid leukemia and prostate cancer .
    BP-1-108
  • HY-178858
    PROTAC FLT3/CHK1 Degrader-1

    		PROTACs FLT3 Checkpoint Kinase (Chk) STAT ERK c-Myc Akt Cancer
    PROTAC FLT3/CHK1 Degrader-1 is a PROTAC FLT3/CHK1 degrader, with DC50 values of 5.88 nM (FLT3) and 4.17 nM (CHK1), respectively. PROTAC FLT3/CHK1 Degrader-1 can inhibit the phosphorylation of FLT3 downstream signaling effectors STAT5 (Tyr694), AKT (Ser473), and ERK (Tyr204), downregulate the protein level of c-Myc and maintain the expression of p53 protein. PROTAC FLT3/CHK1 Degrader-1 induces apoptosis in MV-4-11 cells. PROTAC FLT3/CHK1 Degrader-1 shows significant anti-tumor efficacy in mice bearing MV-4-11 subcutaneous xenografts. PROTAC FLT3/CHK1 Degrader-1 can be used for the study of acute myeloid leukemia (AML). (Pink: FLT3/CHK1 ligand (HY-178869 ), Blue: CRBN Ligand (HY-W093272), Black: Linker, E3 ligase ligand-linker conjugate (HY-W998238)) .
    PROTAC FLT3/CHK1 Degrader-1
  • HY-120457
    WYE-151650

    		JAK STAT Inflammation/Immunology
    WYE-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 .
    WYE-151650
  • HY-153050
    JAK-IN-24

    		JAK Inflammation/Immunology Cancer
    JAK-IN-24 is a JAK inhibitor, with IC50s of 0.534 and 24 nM at the presence of 4 μM or 1mM ATP, respectively. JAK-IN-24 also inhibits PBMC IL-15 induced STAT5 phosphorylation with an IC50 of 86.171 nM . JAK-IN-24 is a click chemistry reagent, it contains an Alkyne group and can undergo copper-catalyzed azide-alkyne cycloaddition (CuAAc) with molecules containing Azide groups.
    JAK-IN-24
  • HY-143286
    PF15

    		PROTACs FLT3 Cancer
    PF15 is a PROTAC connected by ligands for FLT3 kinase and CRBN. PF15 is a high selective FLT3-ITD degrader, with a DC50 of 76.7 nM. PF15 significantly inhibits the proliferation of FLT3-ITD-positive cells, can down-regulate the phosphorylation of FLT3 and STAT5. PF15 also inhibits tumor growth in mouse models and can be used in study of leukemia .
    PF15
  • HY-120604
    BVB808

    NVP_BVB808

    		 JAK STAT Cancer
    BVB808 (NVP_BVB808) is a selective JAK2 inhibitor with approximately 10-fold selectivity for JAK2 over other JAK family members (such as JAK1, JAK3 or TYK2) in vitro. BVB808 inhibits the activity of JAK2 and reduces the phosphorylation of STAT5, thereby blocking the JAK2-dependent cell proliferation and survival signaling pathways. BVB808 can be used in cancer research .
    BVB808
  • HY-116129
    BPR1J-340

    		FLT3 Apoptosis Cancer
    BPR1J-340 is a potent FLT3 inhibitor with an IC50 of ~25 nM. BPR1J-340 inhibits the phosphorylation of FLT3 and STAT5 and triggered apoptosis in FLT3-ITD + acute myeloid leukemia (AML) cells. BPR1J-340 exhibits significant anti-tumor activities .
    BPR1J-340
  • HY-174636
    Human IL15 mRNA

    		mRNA Inflammation/Immunology
    Human IL15 mRNA encodes the human interleukin 15 (IL15) protein, a cytokine that regulates T and natural killer cell activation and proliferation. IL15 induces the activation of JAK kinases, as well as the phosphorylation and activation of transcription activators STAT3, STAT5, and STAT6.
    Human IL15 mRNA
  • HY-168339
    Tyk2-IN-22

    		JAK Inflammation/Immunology
    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 .
    Tyk2-IN-22
  • HY-148522
    FLT3-IN-18

    		FLT3 Cancer
    FLT3-IN-18 is a potent and selective FLT3 inhibitor with an IC50 value of 0.003 μM. FLT3-IN-18 induces apoptosis and cell cycle arrest at G1 phase. FLT3-IN-18 inhibits FLT3 and STAT5 phosphorylation. FLT3-IN-18 has the potential for the research of acute myeloid leukemia (AML) .
    FLT3-IN-18
  • HY-169984S
    Tyk2-IN-22-d3

    		Isotope-Labeled Compounds STAT JAK Inflammation/Immunology
    Tyk2-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 .
    Tyk2-IN-22-d3
  • HY-174437B
    FLT3-IN-32 hydrochloride

    		FLT3 Apoptosis STAT p38 MAPK Akt Cancer
    FLT3-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) .
    FLT3-IN-32 hydrochloride
  • HY-170576
    FLT3-IN-28

    		FLT3 STAT Apoptosis Cancer
    FLT3-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 .
    FLT3-IN-28
  • HY-180969
    SIAIS056

    		PROTACs Bcr-Abl Cancer
    SIAIS056 is a BCR-ABL PROTAC degrader with a DC50 value of 0.18 nM. SIAIS056 time-dependently inhibits the BCR-ABL signaling pathway, accompanied by decreased phosphorylation of BCR-ABL and the downstream molecules STAT5 and CRKL in K562 cells. SIAIS056 induces the degradation of several clinically relevant resistance-conferring mutations of BCR-ABL. SIAIS056 exhibits anti-proliferative activity and induces substantial tumor regression in K562 xenograft models. SIAIS056 can be used for leukemia research .
    SIAIS056
  • HY-179497
    FLT3-IN-37

    		FLT3 VEGFR Akt STAT ERK Apoptosis Cancer
    FLT3-IN-37 (Compound 6z) is a potent inhibitor of FLT3-ITD, with IC50 values of 1.5 and 3.4 nM for FLT3-ITD and TEL-VEGFR2, respectively. FLT3-IN-37 exhibits high selectivity for wild-type FLT3 (WT) and c-Kit. FLT3-IN-37 inhibits FLT3 phosphorylation and downregulates the expression of p-Akt, p-STAT5, and p-ERK. FLT3-IN-37 exerts anti-leukemia effects by blocking the cell cycle and inducing apoptosis (apoptosis). FLT3-IN-37 can be used for research on acute myeloid leukemia (AML) .
    FLT3-IN-37
  • HY-122670
    VS-II-173

    		Pim Apoptosis AMPK DYRK STAT MDM-2/p53 Cancer
    VS-II-173 is a pan-Pim kinase inhibitor with IC50 values ​​of 0.07 μM and 0.02 μM for Pim1 and Pim3, respectively, and a residual activity of 46% for Pim2 at 1 μM. VS-II-173 also inhibits kinases such as HIPK2, PRK2, RSK1, DYRK1a and AMPKα1, selectively inhibiting acute myeloid leukemia (AML) cells with significantly lower toxicity to non-malignant cells (EC50 > 30 μM). VS-II-173 weakens the phosphorylation of substrates such as Stat5 (Y694), MDM2 (S166), Bad (S112), and 4E-BP1 (T37/46) by inhibiting Pim kinase-mediated signaling pathways, blocking pro-survival signals in AML cells and inducing apoptosis. VS-II-173 synergistically enhances anti-AML activity when combined with Daunorubicin (HY-13062A). VS-II-173 can be used in AML research, especially for AML with FLT3-ITD mutations and NPM1 mutations .
    VS-II-173
  • HY-182430
    NVP-BVB808

    		JAK STAT Apoptosis Cancer
    NVP-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 .
    NVP-BVB808

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