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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
21 Results for "
mitochondrial permeability transition pore opening
" in MedChemExpress (MCE) Product Catalog:
Products (21)
21 Results for "mitochondrial permeability transition pore opening" in MCE Product Catalog:
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8 Publications Verification
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Domaines de recherche:
ER-000444793 is a potent inhibitor of mitochondrial permeability transition pore (mPTP) opening. ER-000444793 inhibits mPTP with an IC50 of 2.8 μM.
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Intralipid 20% is a safe fat emulsion, composed of soybean oil (consisting of a mixture of long-chain triglycerides (C14-24) of predominantly unsaturated fatty acids), and egg phospholipids, can be used as a nutritional supplement. Intralipid 20% effectively inhibits the opening of the mitochondrial permeability transition pore, effectively protecting the heart from ischaemia-reperfusion injury and has some potential to modulate the innate immune response .
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Domaines de recherche:
Cardiovascular Disease Metabolic Disease Inflammation/Immunology Cancer
Mocravimod (KRP-203 free base) is a sphingosine-1-phosphate receptor (S1PR) modulator that blocks the signal required by T cells to egress from lymph nodes and other lymphoid organs. Mocravimod preferentially binds to S1PR1 over S1PR2 and S1PR3 in cardiomyocytes. Mocravimod significantly lowered the concentration of reactive oxygen species (ROS), prevented mitochondrial permeability transition pore opening, boosted mitochondrial membrane potential (MMP), and increased phosphorylation of AKT, EKR, GSK-3β, JAK2, and STAT3. Mocravimod retains T cell effector function. Mocravimod can be used for the study of acute myelogenous leukemia, diabetes and Myocardial Ischemia-Reperfusion Injury (MIRI) .
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Mocravimod (hydrochloride) is an orally active sphingosine-1-phosphate receptor (S1PR) modulator that blocks the signal required by T cells to egress from lymph nodes and other lymphoid organs. Mocravimod (hydrochloride) preferentially binds to S1PR1 over S1PR2 and S1PR3 in cardiomyocytes. Mocravimod (hydrochloride) significantly lowered the concentration of reactive oxygen species (ROS), prevented mitochondrial permeability transition pore opening, boosted mitochondrial membrane potential (MMP), and increased phosphorylation of AKT, EKR, GSK-3β, JAK2, and STAT3. Mocravimod (hydrochloride) retains T cell effector function. Mocravimod (hydrochloride) can be used for the study of acute myelogenous leukemia, diabetes and Myocardial Ischemia-Reperfusion Injury (MIRI) .
Cat. No.: HY-N0663
CAS No.: 20501-56-8
Domaines de recherche:
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 .
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Coenzyme Q2 is a benzoquinone electron carrier in the mitochondrial electron transport chain and a p53-dependent apoptosis inducer. Coenzyme Q2 induces p53 phosphorylation at Ser15, promoting p53 accumulation and functional activation. Coenzyme Q2 induces ROS generation, caspase-3 activation, DNA fragmentation, phosphatidylserine externalization, mitochondrial permeability transition pore opening, and oxidative phosphorylation uncoupling. Coenzyme Q2 inhibits Complex I, Complex III, and Complex IV activities, disrupting electron transport and membrane potential generation. Coenzyme Q2 induces excessive mitochondrial proton leak in forebrain mitochondria. Coenzyme Q2 causes loss of righting reflex in mice, accompanied by slow-wave delta EEG activity and reversible loss of wakefulness. Coenzyme Q2 inhibits lipid peroxidation and scavenges superoxide radicals. Coenzyme Q2 is used in research on leukemia, myocardial ischemia-reperfusion injury, and mitochondrial encephalomyopathy .
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-P5288
CAS No.: 184870-31-3
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Cat. No.: HY-172959
CAS No.: 554414-59-4
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mPTP-IN-1 (Compound 14e) is a mitochondrial permeability transition pore (mPTP) inhibitor. mPTP-IN-1 blocks calcium-induced mPTP opening by targeting the C subunit of ATP synthase. mPTP-IN-1 can be used to study myocardial ischemia/reperfusion injury (IRI) .
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-169652
CAS No.: 864860-32-2
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NPC26 is a small molecule mitochondrial disruptor with anti-tumor activity. NPC-26 shows significant anti-proliferative and cytotoxic effects on CRC cell lines (HCT-116, DLD-1, and HT-29). NPC26 can damage mitochondrial function, leading to the opening of the mitochondrial permeability transition pore (mPTP) and the production of reactive oxygen species, ultimately inducing cell death. NPC-26 can kill CRC cells by activating the AMP-activated protein kinase (AMPK) signaling pathway .
Cat. No.: HY-179417
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CypD-IN-7 is a potent cyclophilin D (CypD/PPIF) inhibitor that inhibits CypD PPIase activity (K i = 2.4 nM) and provides protection against mitochondrial permeability transition pore (MPTP) opening. CypD-IN-7 can be used for pancreatitis research .
Cat. No.: HY-L144
1,112 compounds
Normal mitochondrial function is critical for maintaining cellular homeostasis because mitochondria produce ATP and are the major intracellular source of free radicals. Cellular dysfunctions induced by intracellular or extracellular insults converge on mitochondria and induce a sudden increase in permeability on the inner mitochondrial membrane, the so-called mitochondrial membrane permeability transition (MMPT). MMPT is caused by the opening of pores in the inner mitochondrial membrane, matrix swelling, and outer membrane rupture. The MMPT is an endpoint to initiate cell death because the pore opening together with the release of mitochondrial cytochrome c activates the apoptotic pathway of caspases.
The normal operation of mitochondrial function is important for maintaining normal cell death and treatment of mitochondrial diseases. MCE offers a unique collection of 1,112 compounds with identified and potential mitochondrial protective activity. MCE Mitochondrial Protection Compound Library is critical for drug discovery and development.
Cat. No.: HY-100852R
CAS No.: 792957-74-5
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ER-000444793 (Standard) is the analytical standard of ER-000444793 (HY-100852). This product is intended for research and analytical applications. ER-000444793 is a potent inhibitor of mitochondrial permeability transition pore (mPTP) opening. ER-000444793 inhibits mPTP with an IC50 of 2.8 μM.
Cat. No.: HY-P11489
CAS No.: 252731-57-0
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Cat. No.: HY-184943
Domaines de recherche:
Pan-PDK degrader-1 is a pan-PDK class PROTAC degrader that degrades PDK2, PDK3 and PDK4 with DC50 values of 9.2 nM, 9.9 nM and 11.5 nM, respectively. Pan-PDK degrader-1 recruits the mitochondrial protease HsClpP and induces selective pan-PDK degradation via HsClpP-mediated proteolysis. Pan-PDK degrader-1 reprograms mitochondrial metabolism toward oxidative phosphorylation, promoting ROS accumulation, mitochondrial permeability transition pore opening, endogenous mitochondrial apoptosis, calreticulin exposure and HMGB1 release. Pan-PDK degrader-1 upregulates cleaved Caspase-9, Caspase-3 and PARP. Pan-PDK degrader-1 inhibits primary and distal tumor growth via selective degradation of PDK in tumor tissues. Pan-PDK degrader-1 can be used for the research of breast cancer .
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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
