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Results for "

cAMP synthesis

" in MedChemExpress (MCE) Product Catalog:

22

Inhibitors & Agonists

7

Peptides

6

Natural
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1

Isotope-Labeled Compounds

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Art. -Nr. Produktname Target Forschungsgebiete Chemical Structure
  • HY-113402
    Gamma-glutamylcysteine
    4 Publications Verification

    γ-Glu-Cys

    Endogenous Metabolite Interleukin Related TNF Receptor AMPK Sirtuin STAT PI3K NF-κB JAK p38 MAPK JNK Akt Apoptosis Ferroptosis Cardiovascular Disease Neurological Disease Inflammation/Immunology
    Gamma-glutamylcysteine (γ-Glu-Cys) is an orally active, blood-brain barrier permeable dipeptide . Gamma-glutamylcysteine activates AMPK, SIRT1, IL-4/STAT6, AC/cAMP/PI3K, IGF-1R/IRS1/PI3K, and Nrf2 signaling pathways; it inhibits NF-κB, JAK1/STAT1/3, MAPKs, cadmium-induced p38 MAPK, JNK, and PI3K/Akt signaling pathways. Gamma-glutamylcysteine regulates macrophage polarization, modulates the trafficking of CD36 and GLUT4, induces glutathione synthesis, improves metabolic dysfunction, reduces lipid deposition, ameliorates glucose homeostasis, inhibits apoptosis (Apoptosis), stabilizes mitochondria, suppresses lipid peroxidation, iron accumulation and ferroptosis (Ferroptosis), reduces ds-HMGB1 levels, reverses mechanical hyperalgesia, and alleviates hepatic lipid droplet formation. Gamma-glutamylcysteine is applicable to research related to inflammatory bowel disease, type 2 diabetes, cadmium-induced neurotoxicity, Alzheimer's disease, cerebral ischemia/reperfusion injury, neuropathy, and alcoholic liver disease .
    Gamma-glutamylcysteine
  • HY-P1237

    Histamine Receptor Cardiovascular Disease Neurological Disease Metabolic Disease
    C-Type Natriuretic Peptide (CNP) (1-22), human, a 1-22 fragment of CNP, is a natriuretic peptide receptor B (NPR-B) agonist. C-Type Natriuretic Peptide (CNP) (1-22), human inhibits cAMP synthesis stimulated by the physiological agonists histamine and 5-HT or directly by Forskolin. CNP is a potent, endothelial-derived relaxant and growthinhibitory factor .
    C-Type Natriuretic Peptide (CNP) (1-22), human
  • HY-113402A
    Gamma-glutamylcysteine TFA
    4 Publications Verification

    γ-Glu-Cys TFA

    Interleukin Related TNF Receptor Endogenous Metabolite AMPK Sirtuin STAT PI3K NF-κB JAK p38 MAPK JNK Akt Apoptosis Ferroptosis Cardiovascular Disease Neurological Disease Inflammation/Immunology
    Gamma-glutamylcysteine TFA (γ-Glu-Cys TFA) is an orally active, blood-brain barrier permeable dipeptide . Gamma-glutamylcysteine TFA activates AMPK, SIRT1, IL-4/STAT6, AC/cAMP/PI3K, IGF-1R/IRS1/PI3K, and Nrf2 signaling pathways; it inhibits NF-κB, JAK1/STAT1/3, MAPKs, cadmium-induced p38 MAPK, JNK, and PI3K/Akt signaling pathways. Gamma-glutamylcysteine TFA regulates macrophage polarization, modulates the trafficking of CD36 and GLUT4, induces glutathione synthesis, improves metabolic dysfunction, reduces lipid deposition, ameliorates glucose homeostasis, inhibits apoptosis (Apoptosis), stabilizes mitochondria, suppresses lipid peroxidation, iron accumulation and ferroptosis (Ferroptosis), reduces ds-HMGB1 levels, reverses mechanical hyperalgesia, and alleviates hepatic lipid droplet formation. Gamma-glutamylcysteine TFA is applicable to research related to inflammatory bowel disease, type 2 diabetes, cadmium-induced neurotoxicity, Alzheimer's disease, cerebral ischemia/reperfusion injury, neuropathy, and alcoholic liver disease .
    Gamma-glutamylcysteine TFA
  • HY-B0531

    COX Phosphodiesterase (PDE) NF-κB NO Synthase Prostaglandin Receptor Infection Neurological Disease Inflammation/Immunology Cancer
    Triflusal is an orally bioavailable, blood-brain barrier-permeable dual Cyclooxygenase-1 (COX-1)/cAMP phosphodiesterase inhibitor. Triflusal inhibits platelet aggregation, NF-κB activation, iNOS activity, and prostaglandin synthesis in ischaemic tissue. Triflusal stimulates neutrophil nitric oxide production, eNOS protein expression, and cNOS activity. Triflusal alleviates cerebral ischemic injury in rats and ameliorates pathological lesions and related gene expression in transgenic Alzheimer’s disease models. Triflusal can be used for the research of thromboembolic/ischemic cardiovascular and cerebrovascular diseases, and Alzheimer’s disease .
    Triflusal
  • HY-P1291
    PKI 14-22 amide,myristoylated
    3 Publications Verification

    PKA Epigenetic Reader Domain Flavivirus Infection Neurological Disease
    PKI 14-22 amide, myristoylated is a selective, cAMP-dependent, competitive PKA inhibitor with Ki=~36 nM. The myristoylation modification of PKI 14-22 amide, myristoylated makes it more permeable to cell membranes and blood-brain barriers than the precursor molecule. PKI 14-22 amide, myristoylated can block the phosphorylation of cAMP-dependent downstream targets (such as CREB). PKI 14-22 amide, myristoylated can prevent the development of morphine analgesic tolerance in mice, and also inhibits protein translation and negative-strand RNA synthesis of Zika virus. PKI 14-22 amide, myristoylated can be used in research fields such as opioid tolerance mechanisms and antiviral drugs .
    PKI 14-22 amide,myristoylated
  • HY-P0097
    Nonapeptide-1
    2 Publications Verification

    Melanostatine-5

    Melanocortin Receptor Metabolic Disease Endocrinology Cancer
    Nonapeptide-1 (Melanostatine-5), a peptide hormone, is a selective antagonist of MC1R (Ki: 40 nM). Nonapeptide-1 is a competitive α-MSH antagonist that potently inhibits intracellular cAMP and melanosome dispersion induced by α-MSH in melanocytes (IC50: 2.5 nM and 11 nM, respectively). Nonapeptide-1 inhibits melanin synthesis, and can be used in the research of skin pigmentation and regulation of steroid production in the adrenal gland, skin cancer .
    Nonapeptide-1
  • HY-B1428

    Ethenzamide

    Tyrosinase Reactive Oxygen Species (ROS) PERK Neurological Disease Inflammation/Immunology Cancer
    2-Ethoxybenzamide (Ethenzamide) is a nonsteroidal anti-inflammatory agent that shows analgesic and antipyretic effects. 2-Ethoxybenzamide induces melanin synthesis via cAMP response element-binding protein (CREB) phosphorylation. 2-Ethoxybenzamide can be used in the research of hypopigmentation and inflammation-related diseases .
    2-Ethoxybenzamide
  • HY-P1291A
    PKI 14-22 amide,myristoylated TFA
    3 Publications Verification

    PKA Epigenetic Reader Domain Flavivirus Infection Neurological Disease
    PKI 14-22 amide, myristoylated TFA is a selective, cAMP-dependent, competitive PKA inhibitor with Ki=~36 nM. The myristoylation modification of PKI 14-22 amide, myristoylated TFA makes it more permeable to cell membranes and blood-brain barriers than the precursor molecule. PKI 14-22 amide, myristoylated TFA can block the phosphorylation of cAMP-dependent downstream targets (such as CREB). PKI 14-22 amide, myristoylated TFA can prevent the development of analgesic tolerance in mice, and also inhibits protein translation and negative-strand RNA synthesis of Zika virus. PKI 14-22 amide, myristoylated TFA can be used in research fields such as opioid tolerance mechanisms and antiviral drugs .
    PKI 14-22 amide,myristoylated TFA
  • HY-P0097A
    Nonapeptide-1 acetate salt
    2 Publications Verification

    Melanostatine-5 acetate salt

    Melanocortin Receptor Metabolic Disease Endocrinology Cancer
    Nonapeptide-1 (Melanostatine-5) acetate salt, a peptide hormone, is a selective antagonist of MC1R (Ki: 40 nM). Nonapeptide-1 acetate salt is a competitive α-MSH antagonist that potently inhibits intracellular cAMP and melanosome dispersion induced by α-MSH in melanocytes (IC50: 2.5 nM and 11 nM, respectively). Nonapeptide-1 acetate salt inhibits melanin synthesis, and can be used in the research of skin pigmentation and regulation of steroid production in the adrenal gland, skin cancer .
    Nonapeptide-1 acetate salt
  • HY-P1237A

    Histamine Receptor Endothelin Receptor Cardiovascular Disease Neurological Disease Metabolic Disease
    C-Type Natriuretic Peptide (CNP) (1-22), human (TFA),a 1-22 fragment of CNP, is a natriuretic peptide receptor B (NPR-B) agonist. C-Type Natriuretic Peptide (CNP) (1-22), human (TFA) inhibits cAMP synthesis stimulated by the physiological agonists histamine and 5-HT or directly by Forskolin. CNP is a potent, endothelial-derived relaxant and growthinhibitory factor .
    C-Type Natriuretic Peptide (CNP) (1-22), human TFA
  • HY-N6901

    Epigenetic Reader Domain Metabolic Disease
    Luteolin 7-sulfate is isolated from Phyllospadix iwatensis Makino, a marine plant. Luteolin 7-sulfate attenuates TYR gene expression through the intervention of a cAMP-responsive element binding protein (CREB)- and microphthalmia-associated transcription factor (MITF)-mediated signaling pathway, leading to the decreased melanin synthesis .
    Luteolin 7-sulfate
  • HY-P1325

    ((Cys31, Nva 34)-Neuropeptide Y (27-36))2

    Neuropeptide Y Receptor Neurological Disease
    BWX 46 (((Cys31, Nva 34)-Neuropeptide Y (27-36))2) is a selective Y5 receptor agonist with an IC50 value of 0.85 nM. BWX 46 can inhibit the synthesis of cAMP in Y5 cells .
    BWX 46
  • HY-148596

    UDP-N-Acetyl-D-glucosamine; Uridine diphospho-N-acetylglucosamine; UDP-N-acetylglucosamine

    Endogenous Metabolite P2Y Receptor Drug Intermediate Glycosyltransferase Infection
    UDP-GlcNAc (UDP-N-Acetyl-D-glucosamine) is an important component and precursor of bacterial peptidoglycan. UDP-GlcNAc is a nucleotide sugar used by Glycosyltransferases to synthesize glycoproteins, glycosaminoglycans, glycolipids, and glycoRNA. UDP-GlcNAc also serves as the donor substrate for forming O-GlcNAc, a dynamic intracellular protein modification involved in diverse signaling and disease processes. UDP-GlcNAc is the sugar nucleotide donor for the synthesis of O-GlcNAc modified proteins. UDP-GlcNAc also acts as a full agonist of the P2Y14 receptor and inhibits the formation of cAMP. UDP-GlcNAc can be used in studies related to bacterial infections .
    UDP-GlcNAc
  • HY-113402R

    γ-Glu-Cys (Standard)

    Reference Standards Endogenous Metabolite Interleukin Related TNF Receptor AMPK Sirtuin STAT PI3K NF-κB JAK p38 MAPK JNK Akt Apoptosis Ferroptosis Inflammation/Immunology
    Gamma-glutamylcysteine (Standard) is the analytical standard of Gamma-glutamylcysteine. This product is intended for research and analytical applications. Gamma-glutamylcysteine (γ-Glu-Cys) is an orally active, blood-brain barrier permeable dipeptide . Gamma-glutamylcysteine activates AMPK, SIRT1, IL-4/STAT6, AC/cAMP/PI3K, IGF-1R/IRS1/PI3K, and Nrf2 signaling pathways; it inhibits NF-κB, JAK1/STAT1/3, MAPKs, cadmium-induced p38 MAPK, JNK, and PI3K/Akt signaling pathways. Gamma-glutamylcysteine regulates macrophage polarization, modulates the trafficking of CD36 and GLUT4, induces glutathione synthesis, improves metabolic dysfunction, reduces lipid deposition, ameliorates glucose homeostasis, inhibits apoptosis (Apoptosis), stabilizes mitochondria, suppresses lipid peroxidation, iron accumulation and ferroptosis (Ferroptosis), reduces ds-HMGB1 levels, reverses mechanical hyperalgesia, and alleviates hepatic lipid droplet formation. Gamma-glutamylcysteine is applicable to research related to inflammatory bowel disease, type 2 diabetes, cadmium-induced neurotoxicity, Alzheimer's disease, cerebral ischemia/reperfusion injury, neuropathy, and alcoholic liver disease.
    Gamma-glutamylcysteine (Standard)
  • HY-113402AR

    γ-Glu-Cys TFA (Standard)

    Interleukin Related TNF Receptor Endogenous Metabolite Reference Standards AMPK Sirtuin STAT PI3K NF-κB JAK p38 MAPK JNK Akt Apoptosis Ferroptosis Cardiovascular Disease Neurological Disease Inflammation/Immunology
    Gamma-glutamylcysteine (TFA) (Standard) is the analytical standard of Gamma-glutamylcysteine (TFA). This product is intended for research and analytical applications. Gamma-glutamylcysteine TFA (γ-Glu-Cys TFA) is an orally active, blood-brain barrier permeable dipeptide . Gamma-glutamylcysteine TFA activates AMPK, SIRT1, IL-4/STAT6, AC/cAMP/PI3K, IGF-1R/IRS1/PI3K, and Nrf2 signaling pathways; it inhibits NF-κB, JAK1/STAT1/3, MAPKs, cadmium-induced p38 MAPK, JNK, and PI3K/Akt signaling pathways. Gamma-glutamylcysteine TFA regulates macrophage polarization, modulates the trafficking of CD36 and GLUT4, induces glutathione synthesis, improves metabolic dysfunction, reduces lipid deposition, ameliorates glucose homeostasis, inhibits apoptosis (Apoptosis), stabilizes mitochondria, suppresses lipid peroxidation, iron accumulation and ferroptosis (Ferroptosis), reduces ds-HMGB1 levels, reverses mechanical hyperalgesia, and alleviates hepatic lipid droplet formation. Gamma-glutamylcysteine TFA is applicable to research related to inflammatory bowel disease, type 2 diabetes, cadmium-induced neurotoxicity, Alzheimer's disease, cerebral ischemia/reperfusion injury, neuropathy, and alcoholic liver disease.
    Gamma-glutamylcysteine TFA (Standard)
  • HY-B0531S

    Isotope-Labeled Compounds COX NF-κB Phosphodiesterase (PDE) NO Synthase Prostaglandin Receptor Infection Neurological Disease Inflammation/Immunology Cancer
    Triflusal-d3 is deuterium labeled Triflusal (HY-B0531). Triflusal is an orally bioavailable, blood-brain barrier-permeable dual Cyclooxygenase-1 (COX-1)/cAMP phosphodiesterase inhibitor. Triflusal inhibits platelet aggregation, NF-κB activation, iNOS activity, and prostaglandin synthesis in ischaemic tissue. Triflusal stimulates neutrophil nitric oxide production, eNOS protein expression, and cNOS activity. Triflusal alleviates cerebral ischemic injury in rats and ameliorates pathological lesions and related gene expression in transgenic Alzheimer’s disease models. Triflusal can be used for the research of thromboembolic/ischemic cardiovascular and cerebrovascular diseases, and Alzheimer’s disease .
    Triflusal-d3
  • HY-B0531R

    Reference Standards COX Phosphodiesterase (PDE) NF-κB NO Synthase Prostaglandin Receptor Infection Neurological Disease Inflammation/Immunology Cancer
    Triflusal (Standard) is the analytical standard of Triflusal (HY-B0531). This product is intended for research and analytical applications. Triflusal is an orally bioavailable, blood-brain barrier-permeable dual Cyclooxygenase-1 (COX-1)/cAMP phosphodiesterase inhibitor. Triflusal inhibits platelet aggregation, NF-κB activation, iNOS activity, and prostaglandin synthesis in ischaemic tissue. Triflusal stimulates neutrophil nitric oxide production, eNOS protein expression, and cNOS activity. Triflusal alleviates cerebral ischemic injury in rats and ameliorates pathological lesions and related gene expression in transgenic Alzheimer’s disease models. Triflusal can be used for the research of thromboembolic/ischemic cardiovascular and cerebrovascular diseases, and Alzheimer’s disease .
    Triflusal (Standard)
  • HY-B1428R

    Ethenzamide (Standard)

    Reference Standards Tyrosinase Reactive Oxygen Species (ROS) PERK Neurological Disease Inflammation/Immunology Cancer
    2-Ethoxybenzamide (Standard) is the analytical standard of 2-Ethoxybenzamide (HY-B1428). 2-Ethoxybenzamide (Ethenzamide) is a nonsteroidal anti-inflammatory agent that shows analgesic and antipyretic effects. 2-Ethoxybenzamide induces melanin synthesis via cAMP response element-binding protein (CREB) phosphorylation. 2-Ethoxybenzamide can be used in the research of hypopigmentation and inflammation-related diseases .
    2-Ethoxybenzamide (Standard)
  • HY-159917

    Tyrosinase Microtubule/Tubulin Inflammation/Immunology
    PPL agonist-1 is a highly selective Periplakin (PPL) agonist that increases cAMP levels by regulating PPL, thereby enhancing MITF expression and promoting melanin synthesis. Furthermore, PPL agonist-1 facilitates melanin production by regulating tryptophan metabolism. Compared to Ruxolitinib (HY-50856), PPL agonist-1 demonstrates superior efficacy. PPL agonist-1 holds potential for research into vitiligo treatment .
    PPL agonist-1
  • HY-113402B

    γ-Glu-Cys ammonium

    Interleukin Related TNF Receptor Endogenous Metabolite AMPK Sirtuin STAT PI3K NF-κB JAK p38 MAPK JNK Akt Apoptosis Ferroptosis Cardiovascular Disease Neurological Disease Inflammation/Immunology
    Gamma-glutamylcysteine ammonium (γ-Glu-Cys ammonium) is an orally active, blood-brain barrier permeable dipeptide . Gamma-glutamylcysteine ammonium activates AMPK, SIRT1, IL-4/STAT6, AC/cAMP/PI3K, IGF-1R/IRS1/PI3K, and Nrf2 signaling pathways; it inhibits NF-κB, JAK1/STAT1/3, MAPKs, cadmium-induced p38 MAPK, JNK, and PI3K/Akt signaling pathways. Gamma-glutamylcysteine ammonium regulates macrophage polarization, modulates the trafficking of CD36 and GLUT4, induces glutathione synthesis, improves metabolic dysfunction, reduces lipid deposition, ameliorates glucose homeostasis, inhibits apoptosis (Apoptosis), stabilizes mitochondria, suppresses lipid peroxidation, iron accumulation and ferroptosis (Ferroptosis), reduces ds-HMGB1 levels, reverses mechanical hyperalgesia, and alleviates hepatic lipid droplet formation. Gamma-glutamylcysteine ammonium is applicable to research related to inflammatory bowel disease, type 2 diabetes, cadmium-induced neurotoxicity, Alzheimer's disease, cerebral ischemia/reperfusion injury, neuropathy, and alcoholic liver disease .
    Gamma-glutamylcysteine ammonium
  • HY-182503

    Adenosine Kinase Others Inflammation/Immunology
    GP515 is a potent and selective adenosine kinase inhibitor with a human IC50 of 4 nM. GP515 exerts tissue protective effects, produces long-lasting hepatic microcirculation effects after hemorrhagic shock, and induces dose- and time-related VEGF mRNA and protein expression in normoxic rat myocardial myoblasts, with additive VEGF increases during mild hypoxia and no effect during severe hypoxia. GP515 suppresses IFNγ synthesis and CD69 expression in DSS-induced colitis. GP515 also shows a dose-dependent suppression of TNF-α production with an IC50 of 80 μM and can be reversed in the presence of the cAMP antagonist (Rp)-cAMPS. Combinations of GP515 with either adenosine or rolipram led to an additive inhibition of TNF-α synthesis. GP515 can be used for the research of hemorrhagic shock .
    GP515
  • HY-183973

    Thymidylate Synthase Inflammation/Immunology Cancer
    MTXPG5 is a long-chain Methotrexate (HY-14519) metabolite and thymidylate synthase inhibitor with a Ki of 0.047 μM. MTXPG5 inhibits 5-aminoimidazole-4-carboxamide ribonucleotide transformylase, interferes with DNA synthesis and immune cell proliferation, and inhibits pro-inflammatory cytokine production via extracellular adenosine accumulation and elevated cAMP levels. MTXPG5 can be used for the research of leukaemia and rheumatoid arthritis .
    MTXPG5

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