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phosphorylation rate

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22

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2

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Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-N6682
    Cytochalasin D
    90+ Cited Publications

    Zygosporin A; NSC 209835

    		 Exosomes Arp2/3 Complex Antibiotic YAP Infection Cancer
    Cytochalasin D (Zygosporin A) is a potent actin polymerization inhibitor, could be derived from fungus. Cytochalasin D has cell-permeable activity. Cytochalasin D inhibits the G-actin–cofilin interaction by binding to G-actin. Cytochalasin D also inhibits the binding of cofilin to F-actin and decreases the rate of both actin polymerization and depolymerization in living cells. Cytochalasin D can reduce exosome release, in turn reducing the amount of survivin present in the tumour environment. Cytochalasin D induces phosphorylation and cytoplasmic retention of Yap .
    Cytochalasin D
  • HY-13033
    CDK-IN-2
    1 Publications Verification

    CDK inhibitor II

    		 CDK Endocrinology
    CDK-IN-2 is a specific CDK9 inhibitor with an IC50 of less than 8 nM. CDK-IN-2 reduces the phosphorylation level of H3S10. CDK-IN-2 decreases the transition rate of spermatocytes from prophase to metaphase I .
    CDK-IN-2
  • HY-155157
    PF-07247685

    		Endogenous Metabolite Cardiovascular Disease
    PF-07247685 is a BCKDC kinase (BDK) inhibitor (EC50=2.2 nM). PF-07247685 stabilizes the interaction between BDK and BCKDH core subunit E2 and prevents phosphorylation of E1. While BDK mediates branched-chain ketoacid dehydrogenase (BCKDH) phosphorylation, and inhibition of BCKDH is involved in controlling the rate-limiting step of branched-chain amino acid (BCAA) degradation. Impaired BCAA catabolism has been associated with several diseases, particularly cardiometabolic diseases, including heart failure (HF), type 2 diabetes mellitus (T2DM), non-alcoholic fatty liver disease (NAFLD), and obesity. PF-07247685 improved cardiometabolic endpoints and improves glucose tolerance in mice .
    PF-07247685
  • HY-149987
    LY3522348

    KHK-IN-3

    		 Ketohexokinase Cardiovascular Disease Metabolic Disease Inflammation/Immunology
    KHK-IN-3 (Example 1) is a ketohexokinase (KHK) inhibitor. KHK-IN-3 can be used in the study of kidney disease, nonalcoholic steatohepatitis (NASH), diabetes and heart failure. KHK is a rate-limiting enzyme and fructokinase involved in fructose metabolism. KHK catalyzes the phosphorylation of fructose to fructose-1-phosphate (FIP) at the expense of ATP. The lack of feedback inhibition of fructose metabolism triggers the accumulation of downstream intermediates such as lipogenesis, gluconeogenesis, and oxidative phosphorylation .
    LY3522348
  • HY-155554
    SCAL-255

    		Mitochondrial Metabolism Oxidative Phosphorylation Reactive Oxygen Species (ROS) MMP Cancer
    SCAL-255 is a potent mitochondrial complex I (CI) inhibitor with an IC50 of 1.14 μM. SCAL-255 blocks mitochondrial function, inhibits oxygen consumption rate (OCR), induces reactive oxygen species (ROS) production, and reduces MMP. SCAL-255 can be used in the research of oxidative phosphorylation (OXPHOS)-dependent cancers, such as colorectal cancer (CRC) and acute myeloid leukemia (AML), etc .
    SCAL-255
  • HY-A0144A
    Etilefrine hydrochloride

    		Adrenergic Receptor AMPK Akt Cardiovascular Disease
    Etilefrine hydrochloride is a sympathetic nerve agonist and AMPK activator that selectively targets α1/β1 adrenergic receptors. Etilefrine hydrochloride stimulates α1 adrenergic receptors, leading to contraction of vascular smooth muscle and increased peripheral resistance. Etilefrine hydrochloride also stimulates β1 receptors to enhance myocardial contractility and increase heart rate, thereby increasing blood pressure and improving cardiac output. Etilefrine hydrochloride also bidirectionally regulates the AMPK/Akt pathway and modulates the phosphorylation levels. Etilefrine hydrochloride can be used in cardiovascular research, such as postural hypotension, chylothorax, and improving low cardiac output .
    Etilefrine hydrochloride
  • HY-A0144
    Etilefrine

    		Adrenergic Receptor AMPK Akt Cardiovascular Disease
    Etilefrine is a sympathetic nerve agonist and AMPK activator that selectively targets α1/β1 adrenergic receptors. Etilefrine stimulates α1 adrenergic receptors, leading to contraction of vascular smooth muscle and increased peripheral resistance. Etilefrine also stimulates β1 receptors to enhance myocardial contractility and increase heart rate, thereby increasing blood pressure and improving cardiac output. Etilefrine also bidirectionally regulates the AMPK/Akt pathway and modulates the phosphorylation levels. Etilefrine can be used in cardiovascular research, such as postural hypotension, chylothorax, and improving low cardiac output .
    Etilefrine
  • HY-177119
    ZBP1 Covalent PROTAC-1

    		PROTACs RIP kinase Mixed Lineage Kinase Infection Inflammation/Immunology
    ZBP1 Covalent PROTAC-1 is a covalent Z-DNA binding protein 1 ZBP1 PROTAC degrader, with its DC50 being 25.69 nM. ZBP1 Covalent PROTAC-1 integrates the ligand that recruits the VHL E3 ubiquitin ligase and the DNA aptamer (Aptamer Z3) with the specific Zα domain that can bind to ZBP1, which has a high affinity (KD = 2.71 nM) with ZBP1. After degrading ZBP1, the phosphorylation levels of downstream signaling molecules RIPK3 and MLKL significantly decrease. ZBP1 Covalent PROTAC-1, encapsulated by nano-liposomes, significantly improves the survival rate of mice infected with influenza A virus (IAV) after administration via the trachea .
    ZBP1 Covalent PROTAC-1
  • HY-P5522A
    TriDAP dihydrochloride
    1 Publications Verification

    L-Ala-γ-D-Glu-meso-diaminopimelic acid dihydrochloride

    		 NOD-like Receptor (NLR) NF-κB MAP3K MEK ERK p38 MAPK Interleukin Related SARS-CoV Infection Inflammation/Immunology
    TriDAP dihydrochloride (L-Ala-γ-D-Glu-meso-diaminopimelic acid dihydrochloride) is a NOD1 agonist with a Kd value of 34.5 μM. TriDAP dihydrochloride enhances the binding of NOD1-RICK, promotes RICK phosphorylation, and activates the NF-κB, TAK1, MEK/ERK, p38 and interferon response pathways. TriDAP dihydrochloride downregulates Runx2 via increasing ubiquitination and reduces trabecular bone parameters. TriDAP dihydrochloride decreases IκBα levels and increases p65 levels. TriDAP dihydrochloride induces the secretion of proinflammatory mediators IL-8 and prostaglandins, triggers tissue inflammation and innate immune activation, and inhibits SARS-CoV-2 replication in lung epithelial cells. TriDAP dihydrochloride increases the RANKL/OPG ratio in mice, reduces bone mass and enhances osteoclast activity, and inhibits new bone formation by decreasing the mineralization deposition rate in mice. TriDAP dihydrochloride can be used in research related to pulpitis, chronic ulcerative colitis, Crohn's disease and SARS-CoV-2 infection .
    TriDAP dihydrochloride
  • HY-P5522
    TriDAP

    L-Ala-γ-D-Glu-meso-diaminopimelic acid

    		 NOD-like Receptor (NLR) NF-κB MAP3K MEK ERK p38 MAPK Interleukin Related SARS-CoV Infection Inflammation/Immunology
    TriDAP (L-Ala-γ-D-Glu-meso-diaminopimelic acid) is a NOD1 agonist with a Kd value of 34.5 μM. TriDAP enhances the binding of NOD1-RICK, promotes RICK phosphorylation, and activates the NF-κB, TAK1, MEK/ERK, p38 and interferon response pathways. TriDAP downregulates Runx2 via increasing ubiquitination and reduces trabecular bone parameters. TriDAP decreases IκBα levels and increases p65 levels. TriDAP induces the secretion of proinflammatory mediators IL-8 and prostaglandins, triggers tissue inflammation and innate immune activation, and inhibits SARS-CoV-2 replication in lung epithelial cells. TriDAP increases the RANKL/OPG ratio in mice, reduces bone mass and enhances osteoclast activity, and inhibits new bone formation by decreasing the mineralization deposition rate in mice. TriDAP can be used in research related to pulpitis, chronic ulcerative colitis, Crohn's disease and SARS-CoV-2 infection .
    TriDAP
  • HY-155156
    PF-07238025

    		Endogenous Metabolite Cardiovascular Disease
    PF-07238025 is a BCKDC kinase (BDK) inhibitor (EC50=19 nM). PF-07238025 stabilizes the interaction between BDK and BCKDH core subunit E2 and prevents phosphorylation of E1. While BDK mediates branched-chain ketoacid dehydrogenase (BCKDH) phosphorylation, and inhibition of BCKDH is involved in controlling the rate-limiting step of branched-chain amino acid (BCAA) degradation. Impaired BCAA catabolism has been associated with several diseases, particularly cardiometabolic diseases, including heart failure (HF), type 2 diabetes mellitus (T2DM), non-alcoholic fatty liver disease (NAFLD), and obesity. PF-07238025 improved cardiometabolic endpoints and improves glucose tolerance in mice .
    PF-07238025
  • HY-147660
    IMMH001

    		LPL Receptor Inflammation/Immunology
    IMMH001, also called SYL930, is an orally active, potent and selective S1P1 (sphingosine-1-phosphate receptor 1) agonist. IMMH001 decreased levels of both chemokines and proinflammatory cytokines, including IL-1β, IL-5, IL-18, IP10, CCL3, and CCL5. IMMH001 can be used for rheumatoid arthritis (RA) research .
    IMMH001
  • HY-136855
    MitoPBN

    		Sirtuin AMPK PGC-1α Apoptosis Reactive Oxygen Species (ROS) Metabolic Disease
    MitoPBN is a AMPK/SIRT3/PGC-1α axis modulator, reactive oxygen species scavenger and mitochondrial function enhancer. MitoPBN increases the phosphorylation level of AMPK, restores SIRT3 expression and reverses the down-regulation of PGC-1α, thereby promoting mitochondrial biogenesis. MitoPBN regulates glucose metabolism, reduces blood glucose by inhibiting hepatic gluconeogenesis and increasing hepatic glucose uptake, while scavenging mitochondrial superoxide anion/hydrogen peroxide, maintaining membrane potential and increasing ATP production. MitoPBN also reduces cell apoptosis, improves sperm motility, survival rate and membrane integrity, but may induce reductive stress in cryopreserved sperm at high concentrations. MitoPBN is widely applicable to research related to diabetes and type 2 diabetes .
    MitoPBN
  • HY-158178
    EGFR T790M/L858R-IN-7

    		EGFR Cancer
    EGFR T790M/L858R-IN-7 (Compound 72) is a novel pyrimidine compound that inhibits the EGFR T790M and L858R mutation with a high efficacy (93% inhibition rate at 0.05 μM). EGFR T790M/L858R-IN-7 functions by specifically binding to the kinase domain of EGFR, thereby inhibiting its phosphorylation activity .
    EGFR T790M/L858R-IN-7
  • HY-A0144R
    Etilefrine (Standard)

    		Adrenergic Receptor AMPK Akt Reference Standards Cardiovascular Disease
    Etilefrine (Standard) is the analytical standard of Etilefrine. This product is intended for research and analytical applications. Etilefrine is a sympathetic nerve agonist and AMPK activator that selectively targets α1/β1 adrenergic receptors. Etilefrine stimulates α1 adrenergic receptors, leading to contraction of vascular smooth muscle and increased peripheral resistance. Etilefrine also stimulates β1 receptors to enhance myocardial contractility and increase heart rate, thereby increasing blood pressure and improving cardiac output. Etilefrine also bidirectionally regulates the AMPK/Akt pathway and modulates the phosphorylation levels. Etilefrine can be used in cardiovascular research, such as postural hypotension, chylothorax, and improving low cardiac output .
    Etilefrine (Standard)
  • HY-A0144AR
    Etilefrine hydrochloride (Standard)

    		Reference Standards AMPK Adrenergic Receptor Akt Cardiovascular Disease
    Etilefrine hydrochloride (Standard) is the analytical standard of Etilefrine hydrochloride (HY-A0144A). This product is intended for research and analytical applications. Etilefrine hydrochloride is a sympathetic nerve agonist and AMPK activator that selectively targets α1/β1 adrenergic receptors. Etilefrine hydrochloride stimulates α1 adrenergic receptors, leading to contraction of vascular smooth muscle and increased peripheral resistance. Etilefrine hydrochloride also stimulates β1 receptors to enhance myocardial contractility and increase heart rate, thereby increasing blood pressure and improving cardiac output. Etilefrine hydrochloride also bidirectionally regulates the AMPK/Akt pathway and modulates the phosphorylation levels. Etilefrine hydrochloride can be used in cardiovascular research, such as postural hypotension, chylothorax, and improving low cardiac output .
    Etilefrine hydrochloride (Standard)
  • HY-E70936A
    Glycerokinase, Bacillus stearothermophilus

    		Biochemical Assay Reagents Metabolic Disease
    Glycerokinase, Bacillus stearothermophilus (EC 2.7.1.30) is a phosphotransferase enzyme involved in triglycerides and glycerophospholipids synthesis. Glycerokinase catalyzes tge MgATP-dependent phosphorylation of glycerol to produce sn-glycerol-3-phosphate and is the rate limiting enzyme in the utilization of glycerol.
    Glycerokinase, Bacillus stearothermophilus
  • HY-E70936B
    Glycerokinase, Cellulomonas sp.

    		Biochemical Assay Reagents Metabolic Disease
    Glycerokinase, Cellulomonas sp. (EC 2.7.1.30) is a phosphotransferase enzyme involved in triglycerides and glycerophospholipids synthesis. Glycerokinase catalyzes tge MgATP-dependent phosphorylation of glycerol to produce sn-glycerol-3-phosphate and is the rate limiting enzyme in the utilization of glycerol.
    Glycerokinase, Cellulomonas sp.
  • HY-E70936C
    Glycerokinase, Escherichia coli

    		Biochemical Assay Reagents Metabolic Disease
    Glycerokinase, Escherichia coli (EC 2.7.1.30) is a phosphotransferase enzyme involved in triglycerides and glycerophospholipids synthesis. Glycerokinase catalyzes tge MgATP-dependent phosphorylation of glycerol to produce sn-glycerol-3-phosphate and is the rate limiting enzyme in the utilization of glycerol.
    Glycerokinase, Escherichia coli
  • HY-E70936
    Glycerokinase, Streptomyces canus

    		Endogenous Metabolite Metabolic Disease
    Glycerokinase, Streptomyces canus (EC 2.7.1.30) is a phosphotransferase enzyme involved in triglycerides and glycerophospholipids synthesis. Glycerol kinase catalyzes tge MgATP-dependent phosphorylation of glycerol to produce sn-glycerol-3-phosphate and is the rate limiting enzyme in the utilization of glycerol.
    Glycerokinase, Streptomyces canus
  • HY-164111
    JNK-IN-17

    		JAK Neurological Disease
    JNK-IN-17 (Compound 9J) is a selective and potent JNK inhibitor with IC50 values of 0.039, 0.079 μM for JNK1 and JNK3. JNK-IN-17 can inhibit c-Jun phosphorylation with an IC50 of 0.082 μM in Streptozotocin (HY-13753)-infuced INS-1 pancreatic islet β cells. JNK-IN-17 shows inhibition rate ≤ 33% on the four main P450 subtypes (2C9, 2D6, 3A4, 1A2) in human liver microsomes, indicating a relatively low risk of drug interactions. JNK-IN-17 can be used for researches of neurological and metabolic disease, such as Parkinson's disease .
    JNK-IN-17
  • HY-183564
    RIPK1/RIPK3-PPI-IN-1

    		RIP kinase Necroptosis Interleukin Related Inflammation/Immunology
    RIPK1/RIPK3-PPI-IN-1 is an orally active dual-target inhibitor of RIPK1/RIPK3, with a Kd value of 2.4 nM for RIPK1 and 24 nM for RIPK3. RIPK1/RIPK3-PPI-IN-1 inhibits the phosphorylation of RIPK1, RIPK3 and MLKL, thereby suppressing necroptosis. RIPK1/RIPK3-PPI-IN-1 restores body temperature, improves survival rate, and reduces IL-1β/IL-6 levels in serum and multiple organs of Mus musculus, thus alleviating TNF-α-induced systemic inflammatory response syndrome. RIPK1/RIPK3-PPI-IN-1 can be used in research related to systemic inflammatory response syndrome .
    RIPK1/RIPK3-PPI-IN-1

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