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calcium elevation

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24

Inhibitors & Agonists

1

Biochemical Assay Reagents

3

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4

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2

Isotope-Labeled Compounds

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Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-B1272
    Desipramine hydrochloride
    Maximum Cited Publications
    15 Publications Verification

    		 Adrenergic Receptor ERK JNK p38 MAPK NF-κB AP-1 Apoptosis Reactive Oxygen Species (ROS) Mitochondrial Metabolism TNF Receptor Neurological Disease Inflammation/Immunology Cancer
    Desipramine hydrochloride is a first-generation tricyclic antidepressant. Desipramine hydrochloride selectively binds to norepinephrine transporter and blocks neuronal norepinephrine reuptake. Desipramine hydrochloride activates MAPK signaling via ERK1/2, JNK, and p38, represses NF-κB and AP-1 activity, and induces apoptosis via ROS elevation, mitochondrial membrane potential reduction, and intracellular calcium increase. Desipramine hydrochloride also shows anyi-inflammatory activity, inhibiting TNF-α production. Desipramine hydrochloride can be used for the research of hepatocellular cancer, inflammation, and neurological diseases .
    Desipramine hydrochloride
  • HY-B1263
    Chlorobutanol

    		Environmental Pollutants Bacterial Fungal Infection Neurological Disease
    Chlorobutanol is an orally active and potent inhibitor of platelet aggregation and release and a pharmaceutical preservative with antibacterial activity. Chlorobutanol inhibits thromboxane B2 formation, ATP release, and elevation of cytosolic free calcium caused by collagen, ADP, epinephrine, arachidonic acid and thrombin. Chlorobutanol is active against a wide variety of Gram-positive and Gram-negative bacteria, and several mold spores and fungi. Chlorobutanol is widely used in food and cosmetic industry .
    Chlorobutanol
  • HY-113285
    Ureidopropionic acid

    3-Ureidopropionic acid

    		 Oxidative Phosphorylation Metabolic Disease
    Ureidopropionic acid is a mitochondrial respiratory chain complex V inhibitor that selectively inhibits the activity of mitochondrial respiratory chain complex V, with no effect on respiratory chain complexes I-IV or mitochondrial fatty acid β-oxidation. Ureidopropionic acid induces the production of reactive oxygen species, delayed elevation of intracellular calcium concentration, secondary energy-dependent excitotoxicity and neurodegeneration in neurons. Ureidopropionic acid promotes neuropathological changes by impairing mitochondrial energy metabolism, oxidative stress and excitotoxicity pathways. Ureidopropionic acid can be used in studies related to 3-ureidopropionase deficiency and severe propionic aciduria .
    Ureidopropionic acid
  • HY-129724A
    α-MSH (11-13) acetate

    ACTH-(11-13) acetate; Lys-Pro-Val acetate; H-Lys-Pro-Val-OH acetate

    		 Infection Metabolic Disease
    α-MSH (11-13) acetate is a melanocortin-1 receptor ligand and anti-inflammatory agent. α-MSH (11-13) acetate triggers acute intracellular calcium elevation under specific costimulation or pathway inhibition conditions. α-MSH (11-13) acetate inhibits TNF-α-induced NF-κB activation, GPx activity, HIV replication, as well as colony formation of S. aureus and C. albicans. α-MSH (11-13) acetate is applicable to the research of Staphylococcus aureus infection, Candida albicans infection, human immunodeficiency virus infection, traumatic brain injury, corneal epithelial wound and inflammatory bowel disease .
    α-MSH (11-13) acetate
  • HY-Y1667
    2,6-Dibromophenol
    1 Publications Verification

    		 Calcium Channel Fungal Parasite Metabolic Disease
    2,6-Dibromophenol (2,6-DBP) is a weak inhibitor targeting voltage-gated Ca 2+ channels. 2,6-Dibromophenol has no significant effect on potassium-induced calcium elevation in PC12 cells. 2,6-Dibromophenol shows a 48 h EC50 of 2.78 mg/L for Daphnia magna and a 96 h EC50 of 9.90 mg/L for algae (Scenedesmus quadricauda) .
    2,6-Dibromophenol
  • HY-B1035
    Levobunolol hydrochloride
    1 Publications Verification

    l-Bunolol hydrochloride

    		 Adrenergic Receptor Calcium Channel Casein Kinase Cardiovascular Disease
    Levobunolol (l-Bunolol) hydrochloride is a non-selective β-adrenergic antagonist and vasodilator. By blocking calcium ion influx and reducing the sensitivity of vascular smooth muscle to calcium, Levobunolol hydrochloride effectively dilates the ciliary arteries and increases ocular blood flow, so it is widely used in research on glaucoma and ocular hypertension. Levobunolol hydrochloride inhibits the β-receptor signaling pathway and the expression of related proliferation markers (such as CK3, CK14, CK19, Ki67) in corneal cells. In rabbit models, Levobunolol hydrochloride not only does not inhibit corneal epithelial regeneration, but also accelerates the healing of mechanical injury without adverse effects. Levobunolol hydrochloride also inhibits histamine-induced vasoconstriction and intracellular calcium elevation, exhibiting unique vascular regulatory activity. Levobunolol hydrochloride protects ocular blood flow and promotes corneal repair .
    Levobunolol hydrochloride
  • HY-11095
    NPS 2390

    		mGluR CaSR PI3K Akt mTOR Autophagy Apoptosis Bcl-2 Family Caspase Cardiovascular Disease Neurological Disease
    NPS 2390 is an allosteric antagonist of calcium-sensing receptor (CaSR) and mGluR1/5. NPS 2390 inhibits the PI3K/Akt/mTOR signaling pathway, reduces hypoxia-induced intracellular calcium elevation, decreases the expression of autophagy (autophagy) proteins, regulates the expression of phenotypic marker proteins, and inhibits the proliferation of pulmonary artery smooth muscle cells. NPS 2390 attenuates the endogenous apoptosis (apoptosis) pathway, increases the expression level of Bcl-2, downregulates the expression levels of Bax, cytochrome c and caspase-3, alleviates cerebral edema and improves neurological function in rat models. NPS 2390 can be used in studies related to hypoxic pulmonary hypertension, traumatic brain injury, stroke and pain .
    NPS 2390
  • HY-W145486
    Calcium gluconate

    		Environmental Pollutants Biochemical Assay Reagents Neurological Disease Metabolic Disease Inflammation/Immunology
    Calcium gluconate is an orally effective calcium salt supplement . Calcium gluconate reduces elevated serum potassium, decreased serum calcium, and postoperative myalgia associated with succinylcholine administration. Calcium gluconate restores calcium homeostasis, skeletal integrity, bone mineralization and bone density, and maintains levels of parathyroid hormone, bone resorption markers and osteoclasts. Calcium gluconate reverses LPS (HY-D1056)-induced ERK phosphorylation, inflammatory cytokine release and acute lung injury, alleviates airway inflammatory damage and suppresses immune responses. Calcium gluconate can be used in research related to postoperative myalgia, osteoporosis/osteomalacia and acute lung injury .
    Calcium gluconate
  • HY-150270A
    NP-1815-PX sodium

    		P2X Receptor Prostaglandin Receptor NOD-like Receptor (NLR) Caspase Interleukin Related Inflammation/Immunology
    NP-1815-PX sodium is an orally active dual inhibitor of P2X4 and prostaglandin TP receptors, with an IC50 of 0.26 μM against human P2X4 receptors. NP-1815-PX sodium specifically inhibits ATP-mediated prostaglandin production, TP receptor-induced calcium elevation, and the canonical/non-canonical NLRP3 inflammasome signaling pathway. NP-1815-PX sodium selectively blocks smooth muscle contractions induced by ATP, U46619 (HY-108566) and prostaglandin F2α. NP-1815-PX sodium not only produces anti-allodynic effects in vivo, but also significantly alleviates symptoms of DNBS (HY-W324435)-induced colitis (such as weight loss and tissue damage). NP-1815-PX sodium exerts anti-inflammatory effects by downregulating IL-1β levels and Caspase-1 activity. NP-1815-PX sodium is used in studies related to asthma and inflammatory bowel disease (colitis) .
    NP-1815-PX sodium
  • HY-108659
    NF340

    		P2Y Receptor Inflammation/Immunology
    NF340 is a P2Y11 receptor inhibitor with a pIC50 of 7.3-7.7 against human P2Y11 receptor, and it exhibits high selectivity over other P2Y family receptors. NF340 binds to the ATP-binding amino acid residues of the P2Y11 receptor to inhibit its activity, block nociceptive activity, and reduce spinal dorsal horn P2Y11 receptor upregulation induced by spinal cord injury. NF340 attenuates the NFκB signaling pathway activated by IL-1β by decreasing IκBα phosphorylation, nuclear p65 accumulation and NFκB promoter activity. NF340 inhibits IL-1β-induced pro-inflammatory cytokine expression, reduces intracellular ROS and 4-HNE levels, and suppresses IL-1β-induced matrix metalloproteinase expression in primary fibroblast-like synoviocytes. NF340 inhibits ATP-induced elevation of intracellular calcium 2+ concentration and cell migration in human hepatocellular carcinoma cells. NF340 is applicable to the research of neuropathic pain, myocardial ischemia/reperfusion injury, inflammatory pain, rheumatoid arthritis and hepatocellular carcinoma .
    NF340
  • HY-B1272A
    Desipramine

    		Adrenergic Receptor ERK JNK p38 MAPK NF-κB AP-1 Apoptosis Reactive Oxygen Species (ROS) Mitochondrial Metabolism TNF Receptor Neurological Disease Inflammation/Immunology Cancer
    Desipramine is a first-generation tricyclic antidepressant. Desipramine selectively binds to norepinephrine transporter and blocks neuronal norepinephrine reuptake. Desipramine activates MAPK signaling via ERK1/2, JNK, and p38, represses NF-κB and AP-1 activity, and induces apoptosis via ROS elevation, mitochondrial membrane potential reduction, and intracellular calcium increase. Desipramine also shows anyi-inflammatory activity, inhibiting TNF-α production. Desipramine can be used for the research of hepatocellular cancer, inflammation, and neurological diseases .
    Desipramine
  • HY-P5142
    ω-Hexatoxin-Hv1a

    ω-ACTX-Hv1; ω-Atracotoxin-HV1

    		 Insecticide Calcium Channel Apoptosis Necroptosis Cardiovascular Disease Neurological Disease Inflammation/Immunology
    ω-Hexatoxin-Hv1a (ω-ACTX-Hv1; ω-Atracotoxin-HV1) is an orally active insecticidal neurotoxin containing an inhibitor cystine knot motif and a selective calcium channel inhibitor. ω-Hexatoxin-Hv1a blocks L-type voltage-dependent Ca 2+ channels and reduces intracellular calcium ion concentration, thereby decreasing apoptosis, necroptosis and oxidative stress, and promoting cell recovery and energy level elevation. ω-Hexatoxin-Hv1a causes larval paralysis and death by impairing neurotransmission in the central nervous system of insects. It shows high injectable toxicity against insects of multiple orders, but exhibits weak oral toxicity. ω-Hexatoxin-Hv1a is widely applicable to studies related to ischemia-reperfusion injury, atopic dermatitis, and ischemic injury of cardiomyocytes and neurons .
    ω-Hexatoxin-Hv1a
  • HY-124404
    12(R)-HETE

    		Aryl Hydrocarbon Receptor Na+/K+ ATPase Prostaglandin Receptor Inflammation/Immunology
    12(R)-HETE is a CYP-dependent arachidonic acid metabolite that acts as a proinflammatory lipid mediator. 12 (R)-HETE widely exists in various tissues including the eye, skin and liver. In the cornea, 12(R)-HETE is metabolized via pathways such as β-oxidation into the precursor of 12(R)-HETrE. Without direct receptor binding, 12(R)-HETE indirectly activates AHR-mediated target gene transcription, while inhibiting the enzymatic activity of Na+,K+-ATPase and the intracellular calcium elevation induced by TP agonists. 12(R)-HETE also possesses multiple physiological effects such as chemotaxis, proangiogenesis, vasodilation, natriuresis, diuresis and intraocular pressure reduction, and can be widely used in studies related to psoriasis, inflammatory skin diseases and ocular inflammation .
    12(R)-HETE
  • HY-134269A
    8-Br-7-CH-cADPR disodium

    7-deaza-8-bromo-cADPR disodium; 7-deaza-8-bromo-cyclic ADP ribose disodium

    		 Calcium Channel Neurological Disease
    8-Br-7-CH-cADPR disodium (7-Deaza-8-bromo-cADPR) is a potent cADPR antagonist. 8-Br-7-CH-cADPR disodium shows partial inhibition of calcium elevation caused by sTIR dimerization. 8-Br-7-CH-cADPR disodium significantly decreases Paclitaxel (HY-B0015)-induced axon degeneration .
    8-Br-7-CH-cADPR disodium
  • HY-B1272R
    Desipramine hydrochloride (Standard)

    		Reference Standards Adrenergic Receptor ERK JNK p38 MAPK NF-κB AP-1 Apoptosis Reactive Oxygen Species (ROS) Mitochondrial Metabolism TNF Receptor Neurological Disease Inflammation/Immunology Cancer
    Desipramine hydrochloride (Standard) is the analytical standard of Desipramine hydrochloride (HY-B1272). This product is intended for research and analytical applications. Desipramine hydrochloride is a first-generation tricyclic antidepressant. Desipramine hydrochloride selectively binds to norepinephrine transporter and blocks neuronal norepinephrine reuptake. Desipramine hydrochloride activates MAPK signaling via ERK1/2, JNK, and p38, represses NF-κB and AP-1 activity, and induces apoptosis via ROS elevation, mitochondrial membrane potential reduction, and intracellular calcium increase. Desipramine hydrochloride also shows anyi-inflammatory activity, inhibiting TNF-α production. Desipramine hydrochloride can be used for the research of hepatocellular cancer, inflammation, and neurological diseases .
    Desipramine hydrochloride (Standard)
  • HY-150270
    NP-1815-PX

    		Prostaglandin Receptor P2X Receptor NOD-like Receptor (NLR) Caspase Interleukin Related Neurological Disease Inflammation/Immunology
    NP-1815-PX is an orally active dual inhibitor of P2X4 and prostaglandin TP receptors, with an IC50 of 0.26 μM against human P2X4 receptors. NP-1815-PX specifically inhibits ATP-mediated prostaglandin production, TP receptor-induced calcium elevation, and the canonical/non-canonical NLRP3 inflammasome signaling pathway. NP-1815-PX selectively blocks smooth muscle contractions induced by ATP, U46619 (HY-108566) and prostaglandin F2α. NP-1815-PX not only produces anti-allodynic effects in vivo, but also significantly alleviates symptoms of DNBS (HY-W324435)-induced colitis (such as weight loss and tissue damage). NP-1815-PX exerts anti-inflammatory effects by downregulating IL-1β levels and Caspase-1 activity. NP-1815-PX is used in studies related to asthma and inflammatory bowel disease (colitis) .
    NP-1815-PX
  • HY-Y1667R
    2,6-Dibromophenol (Standard)

    		Calcium Channel Fungal Parasite Reference Standards Metabolic Disease
    2,6-Dibromophenol (2,6-DBP) is a weak inhibitor targeting voltage-gated Ca2+ channels. 2,6-Dibromophenol has no significant effect on potassium-induced calcium elevation in PC12 cells. 2,6-Dibromophenol shows a 48 h EC50 of 2.78 mg/L for Daphnia magna and a 96 h EC50 of 9.90 mg/L for algae (Scenedesmus quadricauda) .
    2,6-Dibromophenol (Standard)
  • HY-134269
    8-Br-7-CH-cADPR

    7-Deaza-8-bromo-cADPR; 7-Deaza-8-bromo-cyclic ADP ribose

    		 Calcium Channel Neurological Disease
    8-Br-7-CH-cADPR (7-Deaza-8-bromo-cADPR) is a potent cADPR antagonist. 8-Br-7-CH-cADPR shows partial inhibition of calcium elevation caused by sTIR dimerization. 8-Br-7-CH-cADPR significantly decreases Paclitaxel (HY-B0015)-induced axon degeneration .
    8-Br-7-CH-cADPR
  • HY-B1035A
    Levobunolol

    l-Bunolol

    		 Adrenergic Receptor Casein Kinase Calcium Channel Others
    Levobunolol (l-Bunolol) is a non-selective β-adrenergic antagonist and vasodilator. By blocking calcium ion influx and reducing the sensitivity of vascular smooth muscle to calcium, Levobunolol effectively dilates the ciliary arteries and increases ocular blood flow, so it is widely used in research on glaucoma and ocular hypertension. Levobunolol inhibits the β-receptor signaling pathway and the expression of related proliferation markers (such as CK3, CK14, CK19, Ki67) in corneal cells. In rabbit models, Levobunolol not only does not inhibit corneal epithelial regeneration, but also accelerates the healing of mechanical injury without adverse effects. Levobunolol also inhibits histamine-induced vasoconstriction and intracellular calcium elevation, exhibiting unique vascular regulatory activity. Levobunolol protects ocular blood flow and promotes corneal repair .
    Levobunolol
  • HY-B1272AS
    Desipramine-d4

    		Adrenergic Receptor ERK JNK p38 MAPK NF-κB AP-1 Apoptosis Reactive Oxygen Species (ROS) Mitochondrial Metabolism TNF Receptor Neurological Disease Inflammation/Immunology Cancer
    Desipramine-d4 is the deuterium labeled Desipramine (HY-B1272A). Desipramine is a first-generation tricyclic antidepressant. Desipramine selectively binds to norepinephrine transporter and blocks neuronal norepinephrine reuptake. Desipramine activates MAPK signaling via ERK1/2, JNK, and p38, represses NF-κB and AP-1 activity, and induces apoptosis via ROS elevation, mitochondrial membrane potential reduction, and intracellular calcium increase. Desipramine also shows anyi-inflammatory activity, inhibiting TNF-α production. Desipramine can be used for the research of hepatocellular cancer, inflammation, and neurological diseases .
    Desipramine-d4
  • HY-N3055
    Pinusolide

    		Apoptosis AMPK Platelet-activating Factor Receptor (PAFR) Caspase Neurological Disease Metabolic Disease Cancer
    Pinusolide is an AMPK activator and PAF receptor antagonist. Pinusolide activates AMPK, phosphorylates ACC, enhances IRS-1 tyrosine phosphorylation, boosts glucose uptake, and modulates insulin signaling. Pinusolide inhibits caspase-3/7 activation, intracellular calcium elevation, reactive oxygen species overproduction, lipid peroxidation, and tumor cell proliferation. Pinusolide stabilizes superoxide dismutase activity, reduces apoptotic hallmarks, induces mitochondrial pathway apoptosis, and triggers DNA fragmentation. Pinusolide can be used for the research of type 2 diabetes, neurodegenerative diseases, acute lymphoblastic leukemia, acute myeloid leukemia, and Burkitt lymphoma .
    Pinusolide
  • HY-B1272AS1
    Desipramine-d3

    		Isotope-Labeled Compounds Adrenergic Receptor ERK JNK p38 MAPK NF-κB AP-1 Apoptosis Reactive Oxygen Species (ROS) Mitochondrial Metabolism TNF Receptor Neurological Disease Inflammation/Immunology Cancer
    Desipramine-d3 is the deuterium labeled Desipramine (HY-B1272A). Desipramine is a first-generation tricyclic antidepressant. Desipramine selectively binds to norepinephrine transporter and blocks neuronal norepinephrine reuptake. Desipramine activates MAPK signaling via ERK1/2, JNK, and p38, represses NF-κB and AP-1 activity, and induces apoptosis via ROS elevation, mitochondrial membrane potential reduction, and intracellular calcium increase. Desipramine also shows anyi-inflammatory activity, inhibiting TNF-α production. Desipramine can be used for the research of hepatocellular cancer, inflammation, and neurological diseases .
    Desipramine-d3
  • HY-108942
    ASP5854

    		Adenosine Receptor Cardiovascular Disease Neurological Disease
    ASP5854 is an orally active, blood-brain barrier permeable adenosine A1/A2a dual receptor antagonist. ASP5854 blocks receptor activity and agonist-induced intracellular calcium elevation, and exhibits the characteristic of slow dissociation from striatal A2a receptors in primates. ASP5854 reverses catalepsy, enhances cognitive ability, improves motor function and exerts neuroprotective effects, while also alleviating dyskinesia and increasing contralateral turning behavior. ASP5854 is mainly used in studies related to ischemic stroke and Parkinson's disease .
    ASP5854
  • HY-P5142A
    ω-Hexatoxin-Hv1a TFA

    ω-ACTX-Hv1 TFA; ω-Atracotoxin-HV1 TFA

    		 Insecticide Apoptosis Calcium Channel Necroptosis Cardiovascular Disease Neurological Disease Inflammation/Immunology
    ω-Hexatoxin-Hv1a (ω-ACTX-Hv1; ω-Atracotoxin-HV1) TFA is an orally active insecticidal neurotoxin containing an inhibitor cystine knot motif and a selective calcium channel inhibitor. ω-Hexatoxin-Hv1a TFA blocks L-type voltage-dependent Ca 2+ channels and reduces intracellular calcium ion concentration, thereby decreasing apoptosis, necroptosis and oxidative stress, and promoting cell recovery and energy level elevation. ω-Hexatoxin-Hv1a TFA causes larval paralysis and death by impairing neurotransmission in the central nervous system of insects. It shows high injectable toxicity against insects of multiple orders, but exhibits weak oral toxicity. ω-Hexatoxin-Hv1a TFA is widely applicable to studies related to ischemia-reperfusion injury, atopic dermatitis, and ischemic injury of cardiomyocytes and neurons .
    ω-Hexatoxin-Hv1a TFA

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