149 Results for "

Cell aging

" in MedChemExpress (MCE) Product Catalog:
Products (149)

149 Results for "Cell aging" in MCE Product Catalog:

Cat. No.: HY-B1953S
CAS No.: 1793071-39-2
Thiacloprid-d4 is the deuterium labeled Thiacloprid. Thiacloprid is an orally active neurotoxic insecticide and also a nAChR agonist. Thiacloprid reduces the viability of healthy cells, depletes reduced glutathione, and increases MDA levels, thereby inducing cytotoxicity and oxidative stress damage. In practical applications, Thiacloprid has lower acute toxicity to honeybees than other compounds of the same class such as Imidacloprid (HY-B0838), but it still significantly impairs the learning and memory function, immune capacity and survival status of honeybees. Thiacloprid induces intestinal microbial dysbiosis and reduces survival rate in middle-aged honeybees, increases the risk of premature collapse in bumblebee colonies, and significantly decreases the final colony weight and reproductive output. Thiacloprid is used in broad-spectrum agricultural pest control, often alone or in combination with Deltamethrin (HY-B1971), and meets the pest management needs of various crops including potatoes, cabbages, various fruits and vegetables, and nuts .
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Cat. No.: HY-N7832R
CAS No.: 6988-81-4
Petunidin-3-O-glucoside chloride (Standard) is the analytical standard of Petunidin-3-O-glucoside chloride (HY-N7832). This product is intended for research and analytical applications. Petunidin-3-O-glucoside chloride is a blood-brain barrier-penetrating tyrosinase inhibitor with an IC50 of 10.3 μM and a Ki of 9.0 μM. Petunidin-3-O-glucoside also acts as an α-glucosidase inhibitor with an IC50 of 218.2 µM. Petunidin-3-O-glucoside chloride inhibits the SIRT3/p53-mediated mitochondrial pathway and the PI3K/Akt-ERK pathway, suppresses glycolysis, and induces cell apoptosis. Petunidin-3-O-glucoside chloride scavenges ROS to exert antioxidant activity. It can be used in research related to glioblastoma multiforme, skin anti-aging and whitening, as well as obesity .
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Cat. No.: HY-W089800
CAS No.: 18829-56-6
Synonyms: trans-2-Nonen-1-al
trans-2-Nonenal (trans-2-Nonen-1-al) is an endogenous peroxidation product of polyunsaturated fatty acids, acting as an inhibitor of COX and 12-LOX, as well as an inducer of apoptosis. trans-2-Nonenal is also a malodorous compound secreted by the human body, and its content gradually increases with aging. trans-2-Nonenal inhibits the activities of multiple enzymes such as platelet membrane-bound PTPase, preferentially covalently modifies proteins at lysine residues to form immunogenic adducts, and regulates platelet Arachidonic acid (HY-109590) metabolism. trans-2-Nonenal also exhibits significant cytotoxicity, reduces the viability of keratinocytes, promotes their apoptosis, and effectively decreases the thickness of epidermal models and the number of proliferating cells. trans-2-Nonenal is commonly used in studies of thrombotic, atherosclerotic diseases, renal adenocarcinoma, etc. .
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Cat. No.: HY-160906
CAS No.: 32607-79-7
Synonyms: GSSSG
Glutathione trisulfide (GSSSG) is an orally active, blood-brain barrier permeable neuroprotective agent. Glutathione trisulfide inactivates intracellular tyrosinase, regulates the expression of Cars2, Cbs, MITF and TYR, inhibits α-MSH (HY-P0252)-induced melanogenesis, and restores intracellular persulfide levels reduced by α-MSH. Glutathione trisulfide scavenges free radicals, quenches ROS, reduces Paclitaxel (HY-B0015)-induced superoxide production, upregulates the expression of antioxidant protein genes, and inhibits oxidative stress-induced cell death. Glutathione trisulfide promotes ERK1/2 activation, prevents NF-κB p65 activation, inhibits TAK1 phosphorylation, reduces pro-inflammatory cytokine expression, and blocks microglial activation. Glutathione trisulfide can be used in research related to dry age-related macular degeneration, inflammation-associated eye diseases, Alzheimer's disease, Parkinson's disease, etc.
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Cat. No.: HY-160906A
Synonyms: GSSSG TFA
Glutathione trisulfide TFA (GSSSG TFA) is an orally active, blood-brain barrier permeable neuroprotective agent. Glutathione trisulfide TFA inactivates intracellular tyrosinase, regulates the expression of Cars2, Cbs, MITF and TYR, inhibits α-MSH (HY-P0252)-induced melanogenesis, and restores intracellular persulfide levels reduced by α-MSH. Glutathione trisulfide TFA scavenges free radicals, quenches ROS, reduces Paclitaxel (HY-B0015)-induced superoxide production, upregulates the expression of antioxidant protein genes, and inhibits oxidative stress-induced cell death. Glutathione trisulfide TFA promotes ERK1/2 activation, prevents NF-κB p65 activation, inhibits TAK1 phosphorylation, reduces pro-inflammatory cytokine expression, and blocks microglial activation. Glutathione trisulfide TFA can be used in research related to dry age-related macular degeneration, inflammation-associated eye diseases, Alzheimer's disease, Parkinson's disease, etc.
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Cat. No.: HY-B1953R
CAS No.: 111988-49-9
Research Areas:  

Infection

Thiacloprid (Standard) is the analytical standard of Thiacloprid. This product is intended for research and analytical applications. Thiacloprid is an orally active neurotoxic insecticide and also a nAChR agonist. Thiacloprid reduces the viability of healthy cells, depletes reduced glutathione, and increases MDA levels, thereby inducing cytotoxicity and oxidative stress damage. In practical applications, Thiacloprid has lower acute toxicity to honeybees than other compounds of the same class such as Imidacloprid (HY-B0838), but it still significantly impairs the learning and memory function, immune capacity and survival status of honeybees. Thiacloprid induces intestinal microbial dysbiosis and reduces survival rate in middle-aged honeybees, increases the risk of premature collapse in bumblebee colonies, and significantly decreases the final colony weight and reproductive output. Thiacloprid is used in broad-spectrum agricultural pest control, often alone or in combination with Deltamethrin (HY-B1971), and meets the pest management needs of various crops including potatoes, cabbages, various fruits and vegetables, and nuts .
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Cat. No.: HY-179041
CAS No.: 924851-91-2
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 .
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Cat. No.: HY-L003
3,650 compounds

Apoptosis is an ordered and orchestrated cellular process that occurs in physiological and pathological conditions, which is also called programmed cell death (PCD). Apoptosis plays a crucial role in developing and maintaining the health of the body by eliminating old cells, unhealthy cells and unnecessary cells. Too little or too much apoptosis contribute to many diseases. When apoptosis does not work correctly, cells that should be eliminated may persist and become immortal, for example, in cancer and leukemia. When apoptosis works overly well, it kills too many cells and inflicts grave tissue damage. This is the case in strokes and neurodegenerative disorders such as Alzheimer's, Huntington's, and Parkinson's disease.

MCE designs a unique collection of 3,650 apoptosis-related compounds mainly focusing on the key targets in the apoptosis signaling pathway and can be used in the research of apoptosis signal pathway and related diseases.

Cat. No.: HY-L919
27,503 compounds

With the aging population and increasing competitive pressures, neurodegenerative diseases of the central nervous system (CNS) have become a serious medical challenge in modern society, including Parkinson's disease, Alzheimer's disease, brain tumors, and multiple sclerosis. However, the success rate of CNS drug development remains remarkably low, primarily due to the blood-brain barrier (BBB). The blood-brain barrier (BBB) is a semipermeable barrier structure that surrounds the microvasculature of the CNS. In capillaries, the wedged endothelial cells are tightly packed and wedge-shaped, lining the interior of the vessels to form extensive tight junctions. Along with a range of receptors, transporters, efflux pumps, and other cellular components, this barrier regulates the entry and exit of molecules between the bloodstream and the brain. The intact BBB blocks the passage of most blood-borne substances into the brain, preventing nearly 100% of large-molecule drugs and over 98% of small-molecule drugs from entering. Compared to non-CNS drugs, physicochemical properties such as hydrogen bonds, lipophilicity, and molecular weight significantly influence a compound's ability to cross the BBB. Using artificial intelligence (AI) algorithms to predict BBB permeability, a predicted value greater than 0.75 indicates that the compound has strong potential to cross the BBB, providing a promising starting point for CNS drug discovery.