408 Results for "

integrity

" in MedChemExpress (MCE) Product Catalog:
Products (408)

408 Results for "integrity" in MCE Product Catalog:

Cat. No.: HY-L076
641 compounds

Drug-induced liver injury (DILI; also known as drug-induced hepatotoxicity) is caused by medications (prescription or OTC), herbal and dietary supplements (HDS), or other xenobiotics that result in abnormalities in liver tests or in hepatic dysfunction that cannot be explained by other causes. Drugs are an important cause of liver injury. Drug-induced hepatic injury is the most common reason cited for withdrawal of an approved drug.

DILI is thought to occur via several different mechanisms. Among these are direct impairment of the structural (e.g., mitochondrial dysfunction) and functional integrity of the liver; production of a metabolite that alters hepatocellular structure and function; production of a reactive drug metabolite that binds to hepatic proteins to produce new antigenic drug-protein adducts, which are targeted by hosts’ defenses (the hapten hypothesis); and initiation of a systemic hypersensitivity response (i.e., drug allergy) that damages the liver.

MCE Drug-induced Liver Injury (DILI) Compound Library contains a unique collection of 641 hepatotoxicity causing compounds and is a powerful tool to research DILI and other drug toxicities. This library can be used to understand the mechanisms of DILI, identify biomarkers for early DILI prediction, and allow timely recognition during drug development, thus finally achieving successful DILI prevention and assessment in the pre-marketing phase.

Cat. No.: HY-181926
COX-2/HDAC6-IN-1 (Compound 11e) is a dual COX-2 and HDAC6 inhibitor, with an IC50 of 0.12 μM against HDAC6 and an IC50 of 0.66 μM against COX-2. COX-2/HDAC6-IN-1 enhances the acetylation level of α-tubulin, regulates epigenetic gene expression, and inhibits the expression of pro-inflammatory mediators (COX-2, IL-1β, IL-6 and TNF-α). COX-2/HDAC6-IN-1 promotes Amyloid-β clearance and reduces excessive phosphorylation of Tau protein. COX-2/HDAC6-IN-1 maintains neuronal morphology by stabilizing MAP2, protects synaptic integrity by regulating synapsin, and restores the expression of memory-related genes. COX-2/HDAC6-IN-1 possesses neuroprotective activity and improves learning and memory abilities in Scopolamine (HY-N0296)-induced Alzheimer's disease mouse models. COX-2/HDAC6-IN-1 is applicable to research related to Alzheimer's disease .
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Cat. No.: HY-P10414
Synonyms: KP1 (human)
Target:  

TGF-β Receptor

Research Areas:  

Infection Endocrinology

Klotho-derived peptide 1 (KP1 (human)) is a polypeptide with multiple activities including senescence inhibition and renal protection. Klotho-derived peptide 1 binds to TβR2 and ATAD3A, with a Kd value of 1.41 μM for binding to human TβR2 and a Kd value of 0.319 μM for binding to ATAD3A. By binding to TβR2, Klotho-derived peptide 1 blocks the TGF-β/Smad3 and downstream TGF-β signaling pathways, inhibits the expression of miR-223-3p, induces the expression of lncRNA-TUG1, restores endogenous Klotho at the post-transcriptional level, inhibits cellular senescence markers, fibroblast activation and renal tubular epithelial cell apoptosis, blocks cytochrome c release and caspase activation, maintains the integrity of mitochondrial ultrastructure, and restores mitochondrial protein levels. Klotho-derived peptide 1 enters renal tubular epithelial cells via endocytosis, protects against nephrotoxic and hypoxic injuries, and recapitulates the renal protective and anti-fibrotic effects of full-length Klotho. Klotho-derived peptide 1 can be used in research related to kidney diseases such as chronic kidney disease and SARS-CoV-2-associated acute kidney injury .
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Cat. No.: HY-P10414A
Synonyms: KP1 (human) hydrochloride
Target:  

TGF-β Receptor

Research Areas:  

Infection Endocrinology

Klotho-derived peptide 1 hydrochloride (KP1 (human) hydrochloride) is a polypeptide with multiple activities including senescence inhibition and renal protection. Klotho-derived peptide 1 hydrochloride binds to TβR2 and ATAD3A, with a Kd value of 1.41 μM for binding to human TβR2 and a Kd value of 0.319 μM for binding to ATAD3A. By binding to TβR2, Klotho-derived peptide 1 hydrochloride blocks the TGF-β/Smad3 and downstream TGF-β signaling pathways, inhibits the expression of miR-223-3p, induces the expression of lncRNA-TUG1, restores endogenous Klotho at the post-transcriptional level, inhibits cellular senescence markers, fibroblast activation and renal tubular epithelial cell apoptosis, blocks cytochrome c release and caspase activation, maintains the integrity of mitochondrial ultrastructure, and restores mitochondrial protein levels. Klotho-derived peptide 1 hydrochloride enters renal tubular epithelial cells via endocytosis, protects against nephrotoxic and hypoxic injuries, and recapitulates the renal protective and anti-fibrotic effects of full-length Klotho. Klotho-derived peptide 1 hydrochloride can be used in research related to kidney diseases such as chronic kidney disease and SARS-CoV-2-associated acute kidney injury .
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Cat. No.: HY-W758414
Phoxim-d5 (phenyl-d5) (mixture of isomers) is the deuterated-labeled Phoxim (HY-B0819). Phoxim is an organophosphorus pesticide and an orally active inhibitor of cholinesterase and CYP3A, which induces neurotoxicity in Caenorhabditis elegans and causes nephrotoxicity characterized by glomerular atrophy and interstitial fibrosis. Phoxim induces inhibition of the autophagy pathway. Phoxim induces dopaminergic neuron degeneration and exacerbates Aβ-induced paralysis. Phoxim damages enterocytes and disrupts intestinal barrier integrity. Phoxim induces ROS accumulation. Phoxim induces mitochondrial apoptosis, involving upregulation of Bad, Bax, caspase-3, and caspase-9 and downregulation of Bcl-2. Phoxim inhibits mitochondrial functional enzymes (COX, Ca 2+-Mg 2+-ATPase, SDH). Phoxim upregulates Nrf2 mRNA expression in the jejunal mucosa. Phoxim increases TNF-α and decreases IL-6 and IL-8 in the intestinal mucosa. Phoxim alters gut microbial composition by increasing total bacteria and Escherichia coli and reducing Lactobacillus. Phoxim enhances energy metabolism in silver carp by upregulating key glycolytic and gluconeogenic enzymes. Phoxim is used in research on neurodegenerative diseases, nephrotoxicity, intestinal oxidative stress and barrier dysfunction, and bacterial sepsis .
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Cat. No.: HY-N0113A
CAS No.: 62493-39-4
Synonyms: Ordenina sulfate; Peyocactine sulfate
Hordenine sulfate (Ordenina sulfate; Peyocactine sulfate) is a multifunctional alkaloid with oral activity and blood-brain barrier penetration. Hordenine sulfate inhibits LPS-induced phosphorylation of p38, JNK, ERK1/2, p65, IκB, and AKT, prevents p65 nuclear translocation, and suppresses inflammatory cytokines and mediators. Hordenine sulfate promotes M2 macrophage polarization, restores blood-milk barrier integrity, alleviates oxidative stress by reducing ROS and MDA, and attenuates LPS-induced lung injury and pulmonary edema. Hordenine sulfate inhibits cAMP production, CREB phosphorylation, and MITF expression, thereby suppressing melanin synthesis in melanocytes and reconstructed epidermis. Hordenine sulfate activates the Wnt/β-catenin signaling pathway, promotes dermal papilla cell proliferation and hair shaft elongation, and accelerates hair regeneration. Hordenine sulfate activates DRD2, acts as a D3R partial agonist, α2A-AR full agonist, and 5-HT2A-R antagonist, and inhibits SERT and DAT. Hordenine sulfate inhibits α-synuclein accumulation and ameliorates motor deficits in Parkinson's disease models. Hordenine sulfate limits alcohol intake, reduces relapse drinking behavior, and modulates alcohol-induced conditioned place preference. Hordenine sulfate can be used for research on mastitis, skin pigmentation, acute lung injury, foodborne diseases, hair loss, Parkinson's disease, bacterial infections, and alcohol use disorder .
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Cat. No.: HY-N0113R
CAS No.: 539-15-1
Synonyms: Ordenina (Standard); Peyocactine (Standard)
Hordenine (Standard) (Ordenina (Standard); Peyocactine (Standard)) is the analytical standard of Hordenine (HY-N0113). This product is intended for research and analytical applications. Hordenine (Ordenina; Peyocactine) is a multifunctional alkaloid with oral activity and blood-brain barrier penetration. Hordenine inhibits LPS-induced phosphorylation of p38, JNK, ERK1/2, p65, IκB, and AKT, prevents p65 nuclear translocation, and suppresses inflammatory cytokines and mediators. Hordenine promotes M2 macrophage polarization, restores blood-milk barrier integrity, alleviates oxidative stress by reducing ROS and MDA, and attenuates LPS-induced lung injury and pulmonary edema. Hordenine inhibits cAMP production, CREB phosphorylation, and MITF expression, thereby suppressing melanin synthesis in melanocytes and reconstructed epidermis. Hordenine activates the Wnt/β-catenin signaling pathway, promotes dermal papilla cell proliferation and hair shaft elongation, and accelerates hair regeneration. Hordenine activates DRD2, acts as a D3R partial agonist, α2A-AR full agonist, and 5-HT2A-R antagonist, and inhibits SERT and DAT. Hordenine inhibits α-synuclein accumulation and ameliorates motor deficits in Parkinson's disease models. Hordenine limits alcohol intake, reduces relapse drinking behavior, and modulates alcohol-induced conditioned place preference. Hordenine can be used for research on mastitis, skin pigmentation, acute lung injury, foodborne diseases, hair loss, Parkinson's disease, bacterial infections, and alcohol use disorder .
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Cat. No.: HY-N0113S
CAS No.: 1346598-66-0
Synonyms: Ordenina-d6; Peyocactine-d6
Hordenine-d6 (Ordenina-d6; Peyocactine-d6) is the deuterated-labeled Hordenine (HY-N0113). Hordenine (Ordenina; Peyocactine) is a multifunctional alkaloid with oral activity and blood-brain barrier penetration. Hordenine inhibits LPS-induced phosphorylation of p38, JNK, ERK1/2, p65, IκB, and AKT, prevents p65 nuclear translocation, and suppresses inflammatory cytokines and mediators. Hordenine promotes M2 macrophage polarization, restores blood-milk barrier integrity, alleviates oxidative stress by reducing ROS and MDA, and attenuates LPS-induced lung injury and pulmonary edema. Hordenine inhibits cAMP production, CREB phosphorylation, and MITF expression, thereby suppressing melanin synthesis in melanocytes and reconstructed epidermis. Hordenine activates the Wnt/β-catenin signaling pathway, promotes dermal papilla cell proliferation and hair shaft elongation, and accelerates hair regeneration. Hordenine activates DRD2, acts as a D3R partial agonist, α2A-AR full agonist, and 5-HT2A-R antagonist, and inhibits SERT and DAT. Hordenine inhibits α-synuclein accumulation and ameliorates motor deficits in Parkinson's disease models. Hordenine limits alcohol intake, reduces relapse drinking behavior, and modulates alcohol-induced conditioned place preference. Hordenine can be used for research on mastitis, skin pigmentation, acute lung injury, foodborne diseases, hair loss, Parkinson's disease, bacterial infections, and alcohol use disorder .
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