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Results for "

kidney dysfunction

" in MedChemExpress (MCE) Product Catalog:

18

Inhibitors & Agonists

2

Biochemical Assay Reagents

1

Natural
Products

Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-112879
    Mito-TEMPO
    Maximum Cited Publications
    164 Publications Verification

    		 Calcium Channel PINK1/Parkin Mitochondrial Metabolism Apoptosis Autophagy NOD-like Receptor (NLR) Cardiovascular Disease Neurological Disease Metabolic Disease Inflammation/Immunology
    Mito-TEMPO is a mitochondria-targeted antioxidant. Mito-TEMPO induces mitophagy by activating the PINK1/Parkin pathway, inhibits NLRP3 inflammasome activation, restores mitochondrial membrane potential, and improves renal function and podocyte injury. Mito-TEMPO regulates Ca 2+ homeostasis, inhibits Bnip3 overexpression, shortens action potential duration, and exerts antiarrhythmic effects. Mito-TEMPO reverses premature senescence, reduces trabecular bone loss, and decreases cell apoptosis. Mito-TEMPO can be used in studies of chronic kidney disease, age-related cardiac dysfunction, postmenopausal osteoporosis, and ischemic stroke .
    Mito-TEMPO
  • HY-13687
    IKK 16
    25+ Cited Publications

    		 IKK LRRK2 P-glycoprotein PKD NF-κB TNF Receptor Interleukin Related Cardiovascular Disease Inflammation/Immunology
    IKK 16 is an orally active IKK inhibitor. IKK 16 shows IC50s of 40 nM, 70 nM, 200 nM, and 50 nM for IKK2, IKK complex, IKK1, and LRRK 2, respectively. IKK 16 is also a pan-PKD inhibitor, inhibiting PKD1, PKD2, and PKD3 with IC50s of 153.9, 115, and 99.7 nM, respectively. IKK 16 is also an ABCB1 inhibitor, interfering with the binding of ABCB1 to its substrates. IKK 16 protects against LPS (HY-D1056)-induced multiple organ dysfunction by reducing the acute inflammatory response induced by endotoxin exposure. IKK 16 can restore renal function and alleviate fibrosis in acute kidney injury. IKK 16 attenuates cardiac dysfunction associated with polymicrobial sepsis in mice with type 2 diabetes mellitus (T2DM) by inhibiting the NF-κB pathway .
    IKK 16
  • HY-125944
    MitoTEMPO hydrate
    Maximum Cited Publications
    164 Publications Verification

    		 Mitochondrial Metabolism PINK1/Parkin NOD-like Receptor (NLR) Autophagy Calcium Channel Apoptosis Cardiovascular Disease Neurological Disease Metabolic Disease Endocrinology
    MitoTEMPO hydrate is a mitochondria-targeted antioxidant . MitoTEMPO hydrate induces mitophagy by activating the PINK1/Parkin pathway, inhibits NLRP3 inflammasome activation, restores mitochondrial membrane potential, and improves renal function and podocyte injury. MitoTEMPO hydrate regulates Ca 2+ homeostasis, inhibits Bnip3 overexpression, shortens action potential duration, and exerts antiarrhythmic effects. MitoTEMPO hydrate reverses premature senescence, reduces trabecular bone loss, and decreases cell apoptosis. MitoTEMPO hydrate can be used in studies of chronic kidney disease, age-related cardiac dysfunction, postmenopausal osteoporosis, and ischemic stroke .
    MitoTEMPO hydrate
  • HY-Y0262B
    Sodium oxalate,ACS,99.5%

    Ethanedioic acid sodium,ACS, 99.5%

    		 Environmental Pollutants Biochemical Assay Reagents Mitochondrial Metabolism Metabolic Disease Cancer
    Sodium oxalate is an orally active dispersant and coordination agent. Sodium oxalate causes mitochondrial dysfunction. Sodium oxalate has catalytic enhancing activity. Sodium oxalate induces stable chronic kidney disease. Sodium oxalate induces highly malignant and undifferentiated breast tumors .
    Sodium oxalate,ACS,99.5%
  • HY-144425
    BSc5367

    		NEKs Inflammation/Immunology
    BSc5367 is a potent Nek1 inhibitor with an IC50 of 11.5 nM. NIMA-related protein kinase Nek1 is crucially involved in cell cycle regulation, DNA repair and microtubule regulation and dysfunctions of Nek1 play key roles in amyotrophic lateral sclerosis (ALS), polycystic kidney disease (PKD) and several types of radiotherapy resistant cancer .
    BSc5367
  • HY-13687A
    IKK 16 hydrochloride
    25+ Cited Publications

    		 IKK LRRK2 P-glycoprotein PKD NF-κB TNF Receptor Interleukin Related Cardiovascular Disease Inflammation/Immunology
    IKK 16 hydrochloride is an orally active IKK inhibitor. IKK 16 hydrochloride shows IC50s of 40 nM, 70 nM, 200 nM, and 50 nM for IKK2, IKK complex, IKK1, and LRRK 2, respectively. IKK 16 hydrochloride is also a pan-PKD inhibitor, inhibiting PKD1, PKD2, and PKD3 with IC50s of 153.9, 115, and 99.7 nM, respectively. IKK 16 hydrochloride is also an ABCB1 inhibitor, interfering with the binding of ABCB1 to its substrates. IKK 16 hydrochloride protects against LPS (HY-D1056)-induced multiple organ dysfunction by reducing the acute inflammatory response induced by endotoxin exposure. IKK 16 hydrochloride can restore renal function and alleviate fibrosis in acute kidney injury. IKK 16 hydrochloride attenuates cardiac dysfunction associated with polymicrobial sepsis in mice with type 2 diabetes mellitus (T2DM) by inhibiting the NF-κB pathway .
    IKK 16 hydrochloride
  • HY-116568
    Prothioconazole

    JAU-6476

    		 Fungal Cytochrome P450 Microtubule/Tubulin Mitochondrial Metabolism DNA/RNA Synthesis Apoptosis Fatty Acid Synthase (FASN) Infection Metabolic Disease Endocrinology
    Prothioconazole is an orally active broad-spectrum fungicide. Prothioconazole weakly inhibits CaCYP51 activity in Candida albicans, with an apparent IC50 of approximately 120 μM. Prothioconazole disrupts Microtubule stability by reducing the acetylation level of α-tubulin. Prothioconazole induces Mitochondrial dysfunction, oxidative stress, DNA damage, and Apoptosis. Prothioconazole accumulates 14-methylated sterols and depletes ergosterol in cells, culture media, plants, and animals. Prothioconazole interferes with pyruvate metabolism and glycolysis/gluconeogenesis processes in mouse liver, downregulates Fasn mRNA expression, and induces hepatotoxicity and renal metabolic disorders. Prothioconazole reduces the fertility of female mice. Prothioconazole inhibits body weight gain and increases liver/kidney indices in mice. Prothioconazole can be used in studies related to candidiasis .
    Prothioconazole
  • HY-124283A
    LEI-101

    		Cannabinoid Receptor Neurological Disease
    LEI-101 is a potent, selective, and orally bioavailable cannabinoid CB2 receptor agonist, with a pEC50 of 8 for hCB2, and a pKi of less than 4 for hERG. LEI-101 is ~100-fold more potent in binding to CB2 receptors than to CB1 receptors .
    LEI-101
  • HY-179041
    SZ0232

    		PGE synthase Prostaglandin Receptor MDM-2/p53 Amino acid Transporter Glutathione Peroxidase Ferroptosis Metabolic Disease Endocrinology
    SZ0232 is a selective mPGES-2 inhibitor. SZ0232 binds to the active site of mPGES-2 via hydrogen bonds and π-π stacking, reduces the production of prostaglandin E2 (PGE2) and blocks the PGE2-EP3 pathway. SZ0232 regulates Ferroptosis by activating the heme-dependent p53/SLC7A11/GPX4 axis, inhibits lipid peroxidation, and protects renal tubules. SZ0232 enhances glucose-stimulated insulin secretion, inhibits β-cell senescence, and improves glucose homeostasis. SZ0232 reduces renal lipid accumulation, alleviates fibrosis, and ameliorates renal dysfunction in diabetic mice. SZ0232 inhibits renal cyst growth in polycystic kidney disease models. SZ0232 exhibits an insulinotropic effect that strengthens with the increase of animal age. SZ0232 can be used in studies related to type 2 diabetes, acute kidney injury, diabetic kidney disease, and autosomal dominant polycystic kidney disease .
    SZ0232
  • HY-101410A
    SDMA (p-hydroxyazobenzene-p′-sulfonate)

    Symmetric dimethylarginine (p-hydroxyazobenzene-p′-sulfonate); NG,NG'-Dimethyl-L-arginine (p-hydroxyazobenzene-p′-sulfonate)

    		 Endogenous Metabolite NO Synthase NF-κB Inflammation/Immunology
    SDMA p-hydroxyazobenzene-p′-sulfonate is the p-hydroxyazobenzene-p′-sulfonate salt form of SDMA (HY-101410). SDMA p-hydroxyazobenzene-p′-sulfonate is an endogenous inhibitor of nitric oxide synthase (NO synthase) activity. SDMA p-hydroxyazobenzene-p′-sulfonate is an activator for NF-κB, and promotes the expression of IL-6 and TNF-α. SDMA p-hydroxyazobenzene-p′-sulfonate is stable in serum and plasma, and can be used as a kidney biomarker of hepatic and renal dysfunction .
    SDMA (p-hydroxyazobenzene-p′-sulfonate)
  • HY-13687R
    IKK 16 (Standard)

    		IKK LRRK2 Reference Standards P-glycoprotein PKD NF-κB TNF Receptor Interleukin Related Inflammation/Immunology
    IKK 16 (Standard) is the analytical standard of IKK 16. This product is intended for research and analytical applications. IKK 16 hydrochloride is an orally active IKK inhibitor. IKK 16 hydrochloride shows IC50s of 40 nM, 70 nM, 200 nM, and 50 nM for IKK2, IKK complex, IKK1, and LRRK 2, respectively. IKK 16 hydrochloride is also a pan-PKD inhibitor, inhibiting PKD1, PKD2, and PKD3 with IC50s of 153.9, 115, and 99.7 nM, respectively. IKK 16 hydrochloride is also an ABCB1 inhibitor, interfering with the binding of ABCB1 to its substrates. IKK 16 hydrochloride protects against LPS (HY-D1056)-induced multiple organ dysfunction by reducing the acute inflammatory response induced by endotoxin exposure. IKK 16 hydrochloride can restore renal function and alleviate fibrosis in acute kidney injury. IKK 16 hydrochloride attenuates cardiac dysfunction associated with polymicrobial sepsis in mice with type 2 diabetes mellitus (T2DM) by inhibiting the NF-κB pathway.
    IKK 16 (Standard)
  • HY-149719
    Ferroptosis-IN-4

    		Ferroptosis Metabolic Disease
    Ferroptosis-IN-4 (compound 6k) is a ferroptosis inhibitor with EC50 value of 20 μM. Ferroptosis-IN-4 has no obvious cytotoxicity. Ferroptosis-IN-4 has a protective effect in glycerol-induced RM-AKI mice with alleviating kidney dysfunction .
    Ferroptosis-IN-4
  • HY-149425
    SIRT5 inhibitor 6

    		Sirtuin Inflammation/Immunology Cancer
    SIRT5 Inhibitor 6 is a potent, substrate-competitive and selective SIRT5 inhibitor with an IC50 of 3.0 μM. SIRT5 Inhibitor6 has a therapeutic potential against septic AKI in vivo .
    SIRT5 inhibitor 6
  • HY-180921
    GS-1291269

    		Ketohexokinase Metabolic Disease Endocrinology
    GS-1291269 is a potent and neutral ketohexokinase (KHK) inhibitor, with IC50s of 0.38 and 2.1 nM against KHK-C and KHK-A, respectively. GS-1291269 demonstrates liver and kidney fructose-1-phosphate (F1P) reduction in a fructose challenge model in rats. GS-1291269 can be used for kidney disease and metabolic-dysfunction-associated steatotic liver disease (MASLD) research .
    GS-1291269
  • HY-182294
    HYJ-2

    		URAT1 Metabolic Disease Inflammation/Immunology
    HYJ-2 is a URAT1 inhibitor and urate-lowering agent. HYJ-2 inhibits URAT1-mediated urate transport and interacts with key residues within the URAT1 binding pocket. HYJ-2 reduces serum urate levels in hyperuricemic mice without inducing liver or kidney injury. HYJ-2 shows low cytotoxicity to hepatocytes and renal cells. HYJ-2 does not significantly induce hepatocyte apoptosis or mitochondrial dysfunction. HYJ-2 can be used in studies related to hyperuricemia and gout .
    HYJ-2
  • HY-165504
    Nagstatin

    		Glycosidase Inflammation/Immunology Cancer
    Nagstatin is a naturally derived competitive inhibitor of N-acetyl-β-D-glucosaminidase (NAG-ase), with an IC50 of 0.0012 μg/mL and a Ki of 1.7×10 -8 M against porcine-derived enzyme. Nagstatin enhances cellular immune responses in normal mice and reactivates suppressed cellular immune responses in tumor-bearing mice. Nagstatin can be used in the research of various diseases such as diabetes and leukemia .
    Nagstatin
  • HY-N18656
    Terminalia chebula extract

    		Bacterial Infection
    Terminalia chebula extract, derived from the fruit of the Terminalia chebula tree. Rich in bioactive compounds such as tannins, flavonoids, phenols, and organic acids like gallic acid and ellagic acid, this extract demonstrates a wide range of pharmacological activities. It acts as a natural laxative, supports digestive health, and exhibits potent antioxidant, anti-inflammatory, and antibacterial properties, effectively targeting various pathogenic bacteria, including Helicobacter pylori, Staphylococcus aureus, and Escherichia coli. Terminalia Chebula Extract also shows significant hepatoprotective effects, shielding the liver from damage through antioxidant and anti-inflammatory mechanisms. It has nephroprotective properties, alleviating renal dysfunction and enhancing kidney health by modulating inflammatory pathways. Additionally, the extract demonstrates neuroprotective activity, reducing neuronal damage and improving memory function. It has potential anti-diabetic effects, enhancing glucose uptake and reducing oxidative stress.
    Terminalia chebula extract
  • HY-181413
    PROTAC EZH2 Degrader-44

    		PROTACs Histone Methyltransferase Bcl-2 Family Caspase PARP Cancer
    PROTAC EZH2 Degrader-44 (compound 60) is a highly efficient PROTAC degrader targeting the EZH2-PRC2 complex. By recruiting the CRBN E3 ligase and relying on the proteasome system, PROTAC EZH2 Degrader-44 simultaneously induces the degradation of core components EZH2, SUZ12 and EED, thereby significantly reducing the levels of H3K27me3 and CARM1. PROTAC EZH2 Degrader-44 exerts antiproliferative effects through a dual mechanism: on the one hand, it triggers mitochondrial dysfunction leading to decreased membrane potential; on the other hand, it strongly promotes apoptosis by regulating Bcl-2 family proteins (upregulating Bax, Caspase-3 and PARP, and downregulating Bcl-2). PROTAC EZH2 Degrader-44 exhibits only extremely low cytotoxicity in human normal mammary epithelial, liver and kidney cells, showing a favorable safety window. PROTAC EZH2 Degrader-44 is an ideal tool molecule for exploring the mechanisms of targeted therapy for triple-negative breast cancer .
    PROTAC EZH2 Degrader-44

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