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Targeted therapy! The Capetin Prize winning "Click Chemistry" can be used like this!Targeted therapy! The Nobel Prize winning "Click Chemistry" can be used like this!2025-02-06
30 Results for "
mitochondrial swelling
" in MedChemExpress (MCE) Product Catalog:
Products (30)
30 Results for "mitochondrial swelling" in MCE Product Catalog:
1
1 Cited Publications
Synonyms: (±)-Mevalonolactone; Mevalolactone
Category:
Natural Products Metabolic Disease Endogenous metabolite Disease Research Fields Inflammation/Immunology
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1
1 Cited Publications
Cat. No.: HY-N0859
CAS No.: 69363-14-0
Synonyms: Schizanhenol; Gomisin-K3
Category:
Plant Monophenols Lignans Schisandra chinensis (Turcz.) Baill. Extract Phenols Phenylpropanoids Schisandraceae Extract Disease Research Fields Cancer
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Cat. No.: HY-P3003
CAS No.: 157232-64-9
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Cat. No.: HY-W040128
CAS No.: 70560-51-9
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Kanamycins sulfate is a blood-brain barrier-permeable JNK1 and Bcl-2 modulator as well as an antibiotic, with broad-spectrum antibacterial, and biofilm-inhibiting activities, and it induces autophagy. Kanamycins sulfate promotes Bcl-2 phosphorylation to upregulate autophagy levels, triggering changes such as mitochondrial swelling and endoplasmic reticulum expansion. Consequently, it causes reversible neuronal damage in the dorsal cochlear nucleus without inducing significant neuronal apoptosis. In the presence of exogenous alanine or glucose, Kanamycins sulfate effectively kills drug-resistant bacteria, restores drug sensitivity of multidrug-resistant bacteria, and alleviates urinary tract and kidney infections in mice. Kanamycins sulfate can be applied to scientific research related to Mycobacterium tuberculosis, salmonellosis, brucellosis, shigellosis, urinary tract infections, and reversible neurotoxicity .
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F16 is a mitochondrial permeability transition pore (PTP) modulator with an EC50 of 30 μM in mice. F16 promotes PTP opening, accumulates in cancer cell mitochondria, and induces mitochondrial depolarization, swelling, cristae disruption, outer membrane rupture, ATP depletion, reactive oxygen species (ROS) production, cytochrome c release and mitochondrial uncoupling. F16 induces cell cycle arrest at the G1 (occasionally G2) phase, reduces the phosphotyrosine content of Neu, as well as the levels of phosphorylated PKB/Akt and phosphorylated MAP kinase, downregulates the protein expression levels of Neu and PKB, triggers apoptosis in cells with moderate Bcl-2 expression, and induces necrosis in cells with overexpressed Bcl-2. F16 can be used in research related to breast cancer and gastric cancer .
Cat. No.: HY-W035520
CAS No.: 35369-53-0
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HBED dihydrochloride is an iron-chelating antioxidant. HBED dihydrochloride chelates ferrous iron, promotes its oxidation to ferric iron, and blocks superoxide-driven ferric iron reduction, preventing Haber-Weiss/Fenton hydroxyl radical production. HBED dihydrochloride donates H/electrons, undergoes protonation, reduces radical cations, and forms phenoxyl radicals. HBED dihydrochloride exerts cytoprotective effects against peroxide-induced lung fibroblast injury. HBED dihydrochloride crosses the blood-brain barrier and mitochondrial membrane, exhibits iron affinity/selectivity, and induces iron clearance in iron-loaded monkeys. HBED dihydrochloride reduces hippocampal AQP4, microgliosis, oxidative stress, cerebral edema, and hippocampal swelling, and improves motor function/recovery after traumatic brain injury. HBED dihydrochloride can be used in research on iron overload and traumatic brain injury (TBI) .
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Didesethyl chloroquine (Bisdesethylchloroquine) is the major metabolite of the antimalarial agent Chloroquine (HY-17589A). Didesethyl chloroquine is a potent myocardial inhibitor. Didesethyl chloroquine reduces calcium binding and accumulation in cardiac mitochondria, induces mitochondrial swelling, rupture and membrane conformational changes. Didesethyl chloroquine inhibits the growth of Plasmodium falciparum strains. Didesethyl chloroquine can be used in research related to malaria, chikungunya virus infection, and cardiovascular and cerebrovascular diseases .
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HBED is an iron-chelating antioxidant. HBED chelates ferrous iron, promotes its oxidation to ferric iron, and blocks superoxide-driven ferric iron reduction, preventing Haber-Weiss/Fenton hydroxyl radical production. HBED donates H/electrons, undergoes protonation, reduces radical cations, and forms phenoxyl radicals. HBED exerts cytoprotective effects against peroxide-induced lung fibroblast injury. HBED crosses the blood-brain barrier and mitochondrial membrane, exhibits iron affinity/selectivity, and induces iron clearance in iron-loaded monkeys. HBED reduces hippocampal AQP4, microgliosis, oxidative stress, cerebral edema, and hippocampal swelling, and improves motor function/recovery after traumatic brain injury. HBED can be used in research on iron overload and traumatic brain injury (TBI) .
Cat. No.: HY-P3003S
CAS No.: 1487375-69-8
Synonyms: (±)-Mevalonolactone-d7; Mevalolactone-d7
Cat. No.: HY-P10370
CAS No.: 721397-24-6
Cat. No.: HY-157343
CAS No.: 62010-37-1
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GD3 Ganglioside is an Apoptosis inducer and a biomarker for mouse neural stem cells. GD3 Ganglioside expresses in neural stem cells and the subventricular zone of the adult mouse brain. GD3 Ganglioside targets the mitochondrial permeability transition pore complex, induces pore opening, dissipates mitochondrial transmembrane potential, triggers Mitochondrial swelling, releases pro-apoptotic factors, and activates Caspase-9. GD3 Ganglioside is applicable to research related to glioblastoma .
Cat. No.: HY-157343A
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GD3 Ganglioside sodium is an Apoptosis inducer and biomarker for mouse neural stem cells. GD3 Ganglioside sodium expresses in neural stem cells and the subventricular zone of the adult mouse brain. GD3 Ganglioside sodium targets the mitochondrial permeability transition pore complex, induces pore opening, dissipates mitochondrial transmembrane potential, triggers Mitochondrial swelling, releases pro-apoptotic factors, and activates Caspase-9. GD3 Ganglioside sodium is applicable to research related to glioblastoma .
Cat. No.: HY-157343B
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GD3 Ganglioside ammonium is an Apoptosis inducer and biomarker for mouse neural stem cells. GD3 Ganglioside ammonium expresses in neural stem cells and the subventricular zone of the adult mouse brain. GD3 Ganglioside ammonium targets the mitochondrial permeability transition pore complex, induces pore opening, dissipates mitochondrial transmembrane potential, triggers Mitochondrial swelling, releases pro-apoptotic factors, and activates Caspase-9. GD3 Ganglioside ammonium is applicable to research related to glioblastoma .
Cat. No.: HY-172227
CAS No.: 148089-70-7
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S-15176 is an inhibitor of the mitochondrial permeability transition pore (PTP). S-15176 inhibits mitochondrial swelling induced by tert-butylhydroperoxide with an IC50 value of 45.7 μM. S-15176 inhibits PTP opening, prevents mitochondrial membrane potential dissipation and NAD(P)H oxidation, and increases mitochondrial calcium loading capacity. S-15176 is promising for research of ischemia-reperfusion injury .
Cat. No.: HY-114898
CAS No.: 1826026-00-9
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ML404 (Compound 38) is an inhibitor of the mitochondrial permeability transition pore (mtPTP), which can suppress mitochondrial swelling (EC50=4.9 nM) and only disrupts mitochondrial coupling (an adverse effect) at concentrations > 100 μM. ML404 can be utilized in research related to multiple sclerosis (MS), amyotrophic lateral sclerosis (ALS), Alzheimer's disease (AD), muscular dystrophies (MD), myocardial infarction, and stroke .
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Methoxyflurane (DA-759) is a volatile anesthetic and nephrotoxic agent. Methoxyflurane undergoes defluorination to generate inorganic fluoride and oxalic acid, leading to polyuric renal insufficiency, proximal tubular necrosis, mitochondrial swelling, and ADH-resistant polyuria. Methoxyflurane inhibits Na +/K + ATPase sodium transport. Methoxyflurane is used in research on neurological diseases and kidney diseases .
Cat. No.: HY-114977R
CAS No.: 108605-70-5
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Protocols
Targeted therapy! The Capetin Prize winning "Click Chemistry" can be used like this!Targeted therapy! The Nobel Prize winning "Click Chemistry" can be used like this!A suitable model is crucial in drug screening experiments. Organs can mimic the three-dimensional functional structure of internal organs, have similar spatial organization to corresponding organs, maintain some key characteristics, and reproduce some physiological functions. They are widely used for modeling and personalized drug screening physiological functions.2025-02-06
