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mitochondria dysfunction

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26

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3

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3

Fluorescent Dye

1

Biochemical Assay Reagents

3

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7

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-113402
    Gamma-glutamylcysteine
    4 Publications Verification

    γ-Glu-Cys

    		 Endogenous Metabolite Interleukin Related TNF Receptor AMPK Sirtuin STAT PI3K NF-κB JAK p38 MAPK JNK Akt Apoptosis Ferroptosis Cardiovascular Disease Neurological Disease Inflammation/Immunology
    Gamma-glutamylcysteine (γ-Glu-Cys) is an orally active, blood-brain barrier permeable dipeptide . Gamma-glutamylcysteine activates AMPK, SIRT1, IL-4/STAT6, AC/cAMP/PI3K, IGF-1R/IRS1/PI3K, and Nrf2 signaling pathways; it inhibits NF-κB, JAK1/STAT1/3, MAPKs, cadmium-induced p38 MAPK, JNK, and PI3K/Akt signaling pathways. Gamma-glutamylcysteine regulates macrophage polarization, modulates the trafficking of CD36 and GLUT4, induces glutathione synthesis, improves metabolic dysfunction, reduces lipid deposition, ameliorates glucose homeostasis, inhibits apoptosis (Apoptosis), stabilizes mitochondria, suppresses lipid peroxidation, iron accumulation and ferroptosis (Ferroptosis), reduces ds-HMGB1 levels, reverses mechanical hyperalgesia, and alleviates hepatic lipid droplet formation. Gamma-glutamylcysteine is applicable to research related to inflammatory bowel disease, type 2 diabetes, cadmium-induced neurotoxicity, Alzheimer's disease, cerebral ischemia/reperfusion injury, neuropathy, and alcoholic liver disease .
    Gamma-glutamylcysteine
  • HY-125623
    MitoPerOx
    3 Publications Verification

    		 Fluorescent Dye Others
    MitoPerOx is a mitochondrial-targeted, lipid peroxidation-indicating fluorescent probe with BODIPY581/591 fluorophores. The triphenylphosphine cation (TPP+) of MitoPerOx can be selectively enriched in mitochondria (depending on membrane potential) and can be used to detect lipid peroxidation in the inner mitochondrial membrane. Under the action of lipid peroxides, the BODIPY581/591 fluorophores of MitoPerOx shift their emission wavelength from 590 nm (reduced state) to 520 nm (oxidized state), and ratiometric detection can be performed at an excitation wavelength of 488 nm. MitoPerOx can specifically monitor the peroxidation of mitochondrial phospholipids (especially cardiolipin) and is used in the study of oxidative stress-related diseases (such as aging, neurodegenerative diseases, and mitochondrial dysfunction)[1][2].
    MitoPerOx
  • HY-B0432
    Propafenone
    2 Publications Verification

    SA-79

    		 Sodium Channel Adrenergic Receptor Potassium Channel Cardiovascular Disease Cancer
    Propafenone (SA-79), a sodium-channel blocker, acts an antiarrhythmic agent. Propafenone also has high affinity for the β receptor (IC50=32 nM) . Propafenone blocks the transient outward current (Ito) and the sustained delayed rectifier K current (Isus) with IC50 values of 4.9 μm and 8.6 μm, respectively . Propafenone suppresses esophageal cancer proliferation through inducing mitochondrial dysfunction and induce apoptosis .
    Propafenone
  • HY-113402A
    Gamma-glutamylcysteine TFA
    4 Publications Verification

    γ-Glu-Cys TFA

    		 Interleukin Related TNF Receptor Endogenous Metabolite AMPK Sirtuin STAT PI3K NF-κB JAK p38 MAPK JNK Akt Apoptosis Ferroptosis Cardiovascular Disease Neurological Disease Inflammation/Immunology
    Gamma-glutamylcysteine TFA (γ-Glu-Cys TFA) is an orally active, blood-brain barrier permeable dipeptide . Gamma-glutamylcysteine TFA activates AMPK, SIRT1, IL-4/STAT6, AC/cAMP/PI3K, IGF-1R/IRS1/PI3K, and Nrf2 signaling pathways; it inhibits NF-κB, JAK1/STAT1/3, MAPKs, cadmium-induced p38 MAPK, JNK, and PI3K/Akt signaling pathways. Gamma-glutamylcysteine TFA regulates macrophage polarization, modulates the trafficking of CD36 and GLUT4, induces glutathione synthesis, improves metabolic dysfunction, reduces lipid deposition, ameliorates glucose homeostasis, inhibits apoptosis (Apoptosis), stabilizes mitochondria, suppresses lipid peroxidation, iron accumulation and ferroptosis (Ferroptosis), reduces ds-HMGB1 levels, reverses mechanical hyperalgesia, and alleviates hepatic lipid droplet formation. Gamma-glutamylcysteine TFA is applicable to research related to inflammatory bowel disease, type 2 diabetes, cadmium-induced neurotoxicity, Alzheimer's disease, cerebral ischemia/reperfusion injury, neuropathy, and alcoholic liver disease .
    Gamma-glutamylcysteine TFA
  • HY-W018587
    TBPH

    		Mitochondrial Metabolism Cytochrome P450 TNF Receptor Interleukin Related HSP LDLR Eukaryotic Initiation Factor (eIF) ClpP Metabolic Disease Inflammation/Immunology
    TBPH is a brominated flame retardant. TBPH enhances hepatic steatosis, inflammation, and fibrosis in mice with nonalcoholic steatohepatitis (NASH). TBPH induces dysregulation of phospholipid metabolism, reducing cardiolipin (CL) and phosphatidylserine (PS) levels. TBPH leads to impaired endoplasmic reticulum-mitochondria (ER-Mito) contacts, subsequently causing mitochondrial dysfunction. TBPH induces lung injury through an inflammatory response mediated by mitochondria-derived ds-DNA. TBPH can be used to study the role of MFN2-mediated ER-mitochondria contacts in lipid metabolism homeostasis .
    TBPH
  • 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-DY1073
    MitoPerOx (solution)

    		Fluorescent Dye Others
    MitoPerOx (solution) is a mitochondrial-targeted, lipid peroxidation-indicating fluorescent probe with BODIPY581/591 fluorophores. The triphenylphosphine cation (TPP+) of MitoPerOx can be selectively enriched in mitochondria (depending on membrane potential) and can be used to detect lipid peroxidation in the inner mitochondrial membrane. Under the action of lipid peroxides, the BODIPY581/591 fluorophores of MitoPerOx shift their emission wavelength from 590 nm (reduced state) to 520 nm (oxidized state) , and ratiometric detection can be performed at an excitation wavelength of 488 nm. MitoPerOx can specifically monitor the peroxidation of mitochondrial phospholipids (especially cardiolipin) and is used in the study of oxidative stress-related diseases (such as aging, neurodegenerative diseases, and mitochondrial dysfunction) .
    Solvent and concentration: DMSO: 2 mM
    MitoPerOx (solution)
  • HY-P10409
    SHLP2

    Small humanin-like peptide 2

    		 Apoptosis Reactive Oxygen Species (ROS) Neurological Disease Metabolic Disease
    SHLP2 (Small humanin-like peptide 2) is a small molecule peptide encoded by mitochondrial DNA, belonging to mitochondria derived peptide. SHLP2 has the activity of regulating apoptosis and inhibits cell death. SHLP2 binds to mitochondrial complex 1. SHLP2 improves mitochondrial metabolism by increasing respiration and biogenesis, reducing ROS, and decreasing mtDNA oxidation. SHLP2 also regulated energy homeostasis through the activation of hypothalamic neurons. SHLP2 can be used in the study of diseases related to mitochondrial dysfunction and anti-aging diseases, such as age-related macular degeneration and Parkinson’s disease .
    SHLP2
  • HY-147225
    TSPO Ligand-Linker Conjugates 1

    		AUTACs Mitophagy Neurological Disease Metabolic Disease Cancer
    TSPO Ligand-Linker Conjugates 1 contains a ligand for translocator protein (TSPO) and a linker, which is used for the synthesis of mitochondria-targeting autophagy-targeting chimera (AUTAC). AUTAC can bind the TSPO on the outer mitochondrial membrane (OMM) of mitochondria and degrades impaired mitochondria and proteins via mitophagy, and improves mitochondrial activity. TSPO Ligand-Linker Conjugates 1 can be used in mitochondrial dysfunction related research, including neurodegenerative diseases, cancer, and diabetes .
    TSPO Ligand-Linker Conjugates 1
  • HY-113402R
    Gamma-glutamylcysteine (Standard)

    γ-Glu-Cys (Standard)

    		 Reference Standards Endogenous Metabolite Interleukin Related TNF Receptor AMPK Sirtuin STAT PI3K NF-κB JAK p38 MAPK JNK Akt Apoptosis Ferroptosis Inflammation/Immunology
    Gamma-glutamylcysteine (Standard) is the analytical standard of Gamma-glutamylcysteine. This product is intended for research and analytical applications. Gamma-glutamylcysteine (γ-Glu-Cys) is an orally active, blood-brain barrier permeable dipeptide . Gamma-glutamylcysteine activates AMPK, SIRT1, IL-4/STAT6, AC/cAMP/PI3K, IGF-1R/IRS1/PI3K, and Nrf2 signaling pathways; it inhibits NF-κB, JAK1/STAT1/3, MAPKs, cadmium-induced p38 MAPK, JNK, and PI3K/Akt signaling pathways. Gamma-glutamylcysteine regulates macrophage polarization, modulates the trafficking of CD36 and GLUT4, induces glutathione synthesis, improves metabolic dysfunction, reduces lipid deposition, ameliorates glucose homeostasis, inhibits apoptosis (Apoptosis), stabilizes mitochondria, suppresses lipid peroxidation, iron accumulation and ferroptosis (Ferroptosis), reduces ds-HMGB1 levels, reverses mechanical hyperalgesia, and alleviates hepatic lipid droplet formation. Gamma-glutamylcysteine is applicable to research related to inflammatory bowel disease, type 2 diabetes, cadmium-induced neurotoxicity, Alzheimer's disease, cerebral ischemia/reperfusion injury, neuropathy, and alcoholic liver disease.
    Gamma-glutamylcysteine (Standard)
  • HY-137782
    Palmitoleoyl-CoA

    		Biochemical Assay Reagents Others
    Palmitoleoyl-CoA can be activated and transported into the mitochondria for metabolism, specifically for β-oxidation. Palmitoleoyl-CoA induces the cardiac mitochondrial membrane permeability transition, which causes mitochondrial dysfunction. Palmitoleoyl-CoA regulates metabolism via allosteric control of AMPK β1-isoforms .
    Palmitoleoyl-CoA
  • HY-162344
    Ir-CA

    		Apoptosis Autophagy Cancer
    Ir-CA is an antitumor agent. Ir-CA can accumulate in mitochondria and induces mitochondria dysfunction. Ir-CA induces apoptosis and autophagy. Ir-CA initiates mitophagy and cell cycle arrest to kill Cisplatin (HY-17394)-resistant A549R cells. Ir-CA can effectively inhibit metastasis by inhibiting MMP-2/MMP-9 .
    Ir-CA
  • HY-113402AR
    Gamma-glutamylcysteine TFA (Standard)

    γ-Glu-Cys TFA (Standard)

    		 Interleukin Related TNF Receptor Endogenous Metabolite Reference Standards AMPK Sirtuin STAT PI3K NF-κB JAK p38 MAPK JNK Akt Apoptosis Ferroptosis Cardiovascular Disease Neurological Disease Inflammation/Immunology
    Gamma-glutamylcysteine (TFA) (Standard) is the analytical standard of Gamma-glutamylcysteine (TFA). This product is intended for research and analytical applications. Gamma-glutamylcysteine TFA (γ-Glu-Cys TFA) is an orally active, blood-brain barrier permeable dipeptide . Gamma-glutamylcysteine TFA activates AMPK, SIRT1, IL-4/STAT6, AC/cAMP/PI3K, IGF-1R/IRS1/PI3K, and Nrf2 signaling pathways; it inhibits NF-κB, JAK1/STAT1/3, MAPKs, cadmium-induced p38 MAPK, JNK, and PI3K/Akt signaling pathways. Gamma-glutamylcysteine TFA regulates macrophage polarization, modulates the trafficking of CD36 and GLUT4, induces glutathione synthesis, improves metabolic dysfunction, reduces lipid deposition, ameliorates glucose homeostasis, inhibits apoptosis (Apoptosis), stabilizes mitochondria, suppresses lipid peroxidation, iron accumulation and ferroptosis (Ferroptosis), reduces ds-HMGB1 levels, reverses mechanical hyperalgesia, and alleviates hepatic lipid droplet formation. Gamma-glutamylcysteine TFA is applicable to research related to inflammatory bowel disease, type 2 diabetes, cadmium-induced neurotoxicity, Alzheimer's disease, cerebral ischemia/reperfusion injury, neuropathy, and alcoholic liver disease.
    Gamma-glutamylcysteine TFA (Standard)
  • HY-N2858
    Alpinumisoflavone acetate

    		Apoptosis Cancer
    Alpinumisoflavone acetate is a anticancer agent. Alpinumisoflavone acetate shows antiproliferative activity. Alpinumisoflavone acetate decreases the expression of phosphorylation of ERK1/2. Alpinumisoflavone acetate induces mitochondrial dysfunction and mitochondria-mediated Apoptosis. Alpinumisoflavone acetate has the potential for the research of HCC .
    Alpinumisoflavone acetate
  • HY-168260
    CQ-Mito

    		Apoptosis Ferroptosis MMP Cancer
    CQ-Mito is a Coumarin-Quinazolinone (CQ)-based derivative that targets mitochondria and exhibits profound phototherapeutic performances with an Phototoxic Index (PI) value of 167. CQ-Mito causes cell death by both apoptosis and ferroptosis. CQ-Mito mediates mitochondrial dysfunction, including mitochondrial morphology changed and the loss of MMP. CQ-Mito can efficiently inhibit the tumor growth in organoid tumor models .
    CQ-Mito
  • HY-137782B
    Palmitoleoyl-CoA lithium

    		Biochemical Assay Reagents Others
    Palmitoleoyl-CoA lithium is the lithium salt form of Palmitoleoyl-CoA (HY-137782). Palmitoleoyl-CoA lithium can be activated and transported into the mitochondria for metabolism, specifically for β-oxidation. Palmitoleoyl-CoA lithium induces the cardiac mitochondrial membrane permeability transition, which causes mitochondrial dysfunction. Palmitoleoyl-CoA lithium regulates metabolism via allosteric control of AMPK β1-isoforms .
    Palmitoleoyl-CoA lithium
  • HY-137782A
    Palmitoleoyl-CoA triammonium

    		Biochemical Assay Reagents Others
    Palmitoleoyl-CoA triammonium is the triammonium salt form of Palmitoleoyl-CoA (HY-137782). Palmitoleoyl-CoA triammonium can be activated and transported into the mitochondria for metabolism, specifically for β-oxidation. Palmitoleoyl-CoA triammonium induces the cardiac mitochondrial membrane permeability transition, which causes mitochondrial dysfunction. Palmitoleoyl-CoA triammonium regulates metabolism via allosteric control of AMPK β1-isoforms .
    Palmitoleoyl-CoA triammonium
  • HY-B0432R
    Propafenone (Standard)

    SA-79 (Standard)

    		 Reference Standards Sodium Channel Adrenergic Receptor Potassium Channel Cardiovascular Disease Cancer
    Propafenone (Standard) is the analytical standard of Propafenone. This product is intended for research and analytical applications. Propafenone (SA-79), a sodium-channel blocker, acts an antiarrhythmic agent. Propafenone also has high affinity for the β receptor (IC50=32 nM) . Propafenone blocks the transient outward current (Ito) and the sustained delayed rectifier K current (Isus) with IC50 values of 4.9 μm and 8.6 μm, respectively . Propafenone suppresses esophageal cancer proliferation through inducing mitochondrial dysfunction and induce apoptosis .
    Propafenone (Standard)
  • HY-N8617
    Trijuganone C

    		DNA/RNA Synthesis Caspase PARP Bcl-2 Family Mitochondrial Metabolism Apoptosis Cancer
    Trijuganone C is a tanshinone-type diterpenoid compound. Trijuganone C can be isolated from the roots of Salvia miltiorrhiza Bunge. Trijuganone C induces chromatin condensation, DNA fragmentation, activation of Caspase-3, -8 and -9, as well as cleavage of PARP. Trijuganone C activates Bid and Bax, leading to loss of mitochondrial membrane potential and inducing the release of cytochrome c from mitochondria into the cytosol. Trijuganone C exerts antiproliferative effects through Apoptosis induction mediated by Mitochondrial dysfunction and Caspase activation. Trijuganone C exhibits significant antiproliferative activity against leukemia cells and colon cancer cells .
    Trijuganone C
  • HY-158726
    Complex 3

    		Fluorescent Dye Apoptosis Cancer
    Complex 3 is a fluorescent dithiocarbazate-copper complex with anticancer activity, which localizes to mitochondria. Complex 3 displays excitation/emission maxima of 455-495/535 nm, respectively. Complex 3 inhibits the growth of BxPC-3, AsPC-1, PANC-1, and WI38 pancreatic cancer cells with IC50 values of 0.74, 0.41, 0.62, and 2.06 µM, respectively. Complex 3 induces lipid peroxidation and mitochondrial rupture and shrinkage in AsPC-1 cells. Complex 3 also induces mitochondrial apoptosis and cytokine-cytokine receptor interaction dysfunction in AsPC-1 cells. Complex 3 reduces tumor volume in an AsPC-1 mouse xenograft model .
    Complex 3
  • HY-155719
    fac-[Re(CO)3(L3)(H2O)][NO3]

    		Paraptosis Cancer
    fac-[Re(CO)3(L3)(H2O)][NO3] (compound 3), the rhenium(I) tricarbonyl aqua complex, is an anticancer agent associated with mitochondrial dysfunction. fac-[Re(CO)3(L3)(H2O)][NO3] is cytotoxic to prostate cancer cells with IC50=0.32 μM (PC-3 cells). fac-[Re(CO)3(L3)(H2O)][NO3] mainly accumulates in mitochondria, down-regulates ATP production in PC3 cells, and promotes paraptosis. However, fac-[Re(CO)3(L3)(H2O)][NO3] did not induce necrosis, apoptosis and autophagy .
    fac-[Re(CO)3(L3)(H2O)][NO3]
  • HY-113402B
    Gamma-glutamylcysteine ammonium

    γ-Glu-Cys ammonium

    		 Interleukin Related TNF Receptor Endogenous Metabolite AMPK Sirtuin STAT PI3K NF-κB JAK p38 MAPK JNK Akt Apoptosis Ferroptosis Cardiovascular Disease Neurological Disease Inflammation/Immunology
    Gamma-glutamylcysteine ammonium (γ-Glu-Cys ammonium) is an orally active, blood-brain barrier permeable dipeptide . Gamma-glutamylcysteine ammonium activates AMPK, SIRT1, IL-4/STAT6, AC/cAMP/PI3K, IGF-1R/IRS1/PI3K, and Nrf2 signaling pathways; it inhibits NF-κB, JAK1/STAT1/3, MAPKs, cadmium-induced p38 MAPK, JNK, and PI3K/Akt signaling pathways. Gamma-glutamylcysteine ammonium regulates macrophage polarization, modulates the trafficking of CD36 and GLUT4, induces glutathione synthesis, improves metabolic dysfunction, reduces lipid deposition, ameliorates glucose homeostasis, inhibits apoptosis (Apoptosis), stabilizes mitochondria, suppresses lipid peroxidation, iron accumulation and ferroptosis (Ferroptosis), reduces ds-HMGB1 levels, reverses mechanical hyperalgesia, and alleviates hepatic lipid droplet formation. Gamma-glutamylcysteine ammonium is applicable to research related to inflammatory bowel disease, type 2 diabetes, cadmium-induced neurotoxicity, Alzheimer's disease, cerebral ischemia/reperfusion injury, neuropathy, and alcoholic liver disease .
    Gamma-glutamylcysteine ammonium
  • HY-P10707
    Tpp-CAQK

    		Endogenous Metabolite Inflammation/Immunology
    Tpp-CAQK can bind to mitochondria, enabling the construction of an engineered mitochondrial compound, Mito-Tpp-CAQK, with excellent bioactivity. Mito-Tpp-CAQK can be internalized by macrophages, thereby enhancing the phagocytosis of myelin debris, alleviating mitochondrial dysfunction, and reducing proinflammatory profiles, ultimately facilitating tissue repair and functional recovery in mice after spinal cord injury .
    Tpp-CAQK
  • HY-P10707A
    Tpp-CAQK TFA

    		Endogenous Metabolite Inflammation/Immunology
    Tpp-CAQK TAF can bind to mitochondria, enabling the construction of an engineered mitochondrial compound, Mito-Tpp-CAQK TFA, with excellent bioactivity. Mito-Tpp-CAQK TFA can be internalized by macrophages, thereby enhancing the phagocytosis of myelin debris, alleviating mitochondrial dysfunction, and reducing proinflammatory profiles, ultimately facilitating tissue repair and functional recovery in mice after spinal cord injury .
    Tpp-CAQK TFA
  • HY-182266
    FBP

    		Mitochondrial Metabolism Apoptosis Reactive Oxygen Species (ROS) DNA/RNA Synthesis Cancer
    FBP is a mitochondria-targeted, selective anticancer agent. FBP induces oxidative stress and mitochondrial dysfunction, leading to Apoptosis. FBP generates ROS and causes double-strand DNA breaks in cancer cells. FBP exhibits cytotoxic efficacy against cancer cells, with cervical cancer cells being the most sensitive. FBP can be used for the research of cervical cancer, lung cancer, melanoma and breast cancer .
    FBP

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