2. Signaling Pathways
  3. Metabolic Enzyme/Protease
  4. Mitochondrial Metabolism

Mitochondrial Metabolism

Mitochondrial Metabolism

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Mitochondria use multiple carbon fuels to produce ATP and metabolites, including pyruvate, which is generated from glycolysis; amino acids such as glutamine; and fatty acids. These carbon fuels feed into the TCA cycle in the mitochondrial matrix to generate the reducing equivalents NADH and FADH2, which deliver their electrons to the electron transport chain. Mitochondria are complex organelles that play an important role in many facets of cellular function, from metabolism to immune regulation and cell death. Mitochondria are actively involved in a wide variety of cellular processes and molecular interactions, such as calcium buffering, lipid flux, and intracellular signaling. It is increasingly recognized that mitochondrial dysfunction is a hallmark of many diseases such as obesity/diabetes, cancer, cardiovascular and neurodegenerative diseases. Mitochondrial metabolism is a key determinant of tumor progression by impacting on functions such as epithelial-to-mesenchymal transition. Mitochondrial metabolism and derived oncometabolites shape the epigenetic landscape to alter aggressiveness features of cancer cells. Changes in mitochondrial metabolism are relevant for the survival of tumors in response to therapy.

Cat. No. Product Name Effect Purity Chemical Structure
  • HY-177483
    OART
    OART (Oxaliplatin-artesunate) is a ferroptosis inducer. OART significantly inhibits tumor cell proliferation. OART induces cytoplasmic and mitochondrial LPO to promote tumor ferroptosis, via destroying glutathione-mediated ferroptosis defense system and enhancing iron-dependent Fenton reaction. OART enhances tumor immunogenicity, transforming tumor environment from immunosuppressive to immunosensitive. OART has strong tumor regression in tumor-bearing mouse models. OART can be used for cancer immunotherapy research.
    OART
  • HY-168030
    hCAIX-IN-23
    hCAIX-IN-23 (Compound 27) is a human carbonic anhydrase (hCA) inhibitor with Ki values of 10.4 and 8.5 nM for hCA IX and hCA XII, respectively. In addition to inhibiting hCA activity, hCAIX-IN-23 releases NO, exhibiting dual antitumor activity. hCAIX-IN-23 induces apoptosis by regulating mitochondrial caspase activity and the ferroptosis pathway (ferroptosis) through the downregulation of hCA IX and iron-regulatory protein expression. hCAIX-IN-23 is useful for renal cancer research.
    hCAIX-IN-23
  • HY-145303
    DX2-201
    		Inhibitor
    DX2-201 is a potent and selective oxidative phosphorylation (OXPHOS) complex I inhibitor with an IC50 of 312 nM. DX2-201 has anticancer effects.
    DX2-201
  • HY-125714
    Isoapoptolidin
    		Inhibitor
    Isoapoptolidin is a mitochondrial F0F1-ATPase inhibitor (Ki>100 μM, selective for mitochondrial complex V). Isoapoptolidin is promising for research of mitochondrial energy metabolism-related diseases (e.g., cancer, neurodegeneration).
    Isoapoptolidin
  • HY-167711
    Sirtuin modulator 9
    		Inducer
    Sirtuin modulator 9 (Compound 214) is a sirtuin-modulating compound that may be used to increase lifespan of cells and in diseases related to aging, inflammation and cancer as well as diseases that would benefit from increased mitochondrial activity.
    Sirtuin modulator 9
  • HY-N12887
    Mycothiazole
    		Inhibitor
    Mycothiazole is an inhibitor for mitochondrial electron transport chain (ETC) complex I. Mycothiazole exhibits cytotoxicity in cancer cells Huh7 (IC50 is 55.8 μM), U87 and MCF7. Mycothiazole induces apoptosis in Huh7. Mycothiazole utilizes the unfolded protein response (UPR) and heat shock response (HSR) pathway involved transcription factors ATFS-1 and HSF1, to extend the lifespan of C. elegans.
    Mycothiazole
  • HY-159910
    LH1513
    LH1513 is a dioxalate derivative of l-lysine (HY-N0469) that inhibits CaOx crystallization with better activity than citrate and pyruvate. LH1513 has potential preventive activity in hyperoxaluria models and effectively prevents urinary CaOx crystal formation in Agxt knockout mice. AGXT-1 is a mitochondrial protein involved in metabolism.
    LH1513
  • HY-P11358
    IRW
    		Activator
    IRW is an orally active tripeptide produced from egg white with angiotensin converting enzyme (ACE) inhibitory properties. IRW can prevent high-fat diet (HFD)-induced Non-alcoholic fatty liver disease (NAFLD) by modulating hepatic lipid metabolism and increasing mitochondrial content. IRW decreases hepatic triglyceride content and lipid droplet size. IRW increases the hepatic mitochondrial complexes and citrate synthase activity, phosphorylation of 5’-AMP-activated protein kinase and microsomal triglyceride transfer protein abundance. IRW increases phosphorylated acetyl CoA carboxylase and mitochondrial complexes, IRW can be used for the research of inflammation.
    IRW
  • HY-159518
    ROS inducer 4
    		Inhibitor
    ROS inducer 4 (compound TE3) is a mitochondrial inhibitor. ROS inducer 4 causes a series of mitochondria-related physiological changes in tumors, such as mitochondrial fragmentation, explosive generation and accumulation of ROS, decreased mitochondrial membrane potential, decreased ATP content, and activation of ROS-mediated apoptotic signaling in mitochondria.
    ROS inducer 4
  • HY-121292
    Clidanac
    Clidanac is a potent anti-inflammatory agent. Clidanac can uncouple the oxidative phosphorylation and can be used for the research of rheumatoid arthritis.
    Clidanac
  • HY-150772
    Tubulin/HDAC-IN-1
    Tubulin/HDAC-IN-1 is a dual tubulin and HDAC-IN-1 inhibitor through CH/π interaction with tubulin and hydrogen bond interaction with HDAC8. Tubulin/HDAC-IN-1 inhibits tubulin polymerization and selectively inhibits HDAC8 (IC50: 150 nM). Tubulin/HDAC-IN-1 has cytotoxicity against various human cancer cells, also arrests cell cycle in the G2/M phase and induces cell apoptosis. Tubulin/HDAC-IN-1 can be used in the research of hematologic and solid tumors such as neuroblastoma, leukemia.
    Tubulin/HDAC-IN-1
  • HY-W001187R
    Tempo (Standard)
    Tempo (Standard) is the analytical standard of Tempo. This product is intended for research and analytical applications. Tempo is a nitric oxide radical and a selective scavenger of ROS in mitochondria. Tempo is also an organocatalyst that disproportionates superoxide and oxidizes primary alcohols to aldehydes in a catalytic cycle. Tempo has mutagenic and antioxidant effects and can induceDNA strand breaks. Tempo also exerts cytotoxic and mutagenic properties in mouse lymphoma cells[4].
    Tempo (Standard)
  • HY-115507A
    (Z)-NMac1
    		Inhibitor
    (Z)-NMac1 is an Nm23-H1 activator found in Zingiber cassumunar Roxb. (Z)-NMac1 has dual anti-metastatic and anti-proliferative biological activities. (Z)-NMac1 selectively inhibits cancer cell proliferation under glucose starvation conditions by inhibiting mitochondrial complex I activity, leading to ATP depletion and mitochondrial dysfunction. (Z)-NMac1 can be used to study tumors with high oxidative phosphorylation, especially in the glucose-restricted tumor microenvironment.
    (Z)-NMac1
  • HY-144311
    OXPHOS-IN-1
    		Inhibitor
    OXPHOS-IN-1 (compound 2) is a oxidative phosphorylation (OXPHOS) inhibitor. OXPHOS-IN-1 inhibits the cells growth of MIA PaCa-2 and BxPC-3 cells with IC50s of 2.34 μM and 13.82 μM, respectively.
    OXPHOS-IN-1
  • HY-126222B
    (E/Z)-MitoTam iodide, hydriodide
    		Inhibitor 98.57%
    (E/Z)-MitoTam (iodide, hydriodide) (MitoTam (iodide, hydriodide)) is the E/Z mixture of MitoTam iodide, hydriodide. MitoTam iodide, hydriodide is a Tamoxifen derivative, an electron transport chain (ETC) inhibitor, spreduces mitochondrial membrane potential in senescent cells and affects mitochondrial morphology. MitoTam iodide, hydriodide is an effective anticancer agent, suppresses respiratory complexes (CI-respiration) and disrupts respiratory supercomplexes (SCs) formation in breast cancer cells. MitoTam iodide, hydriodide causes apoptosis.
    (E/Z)-MitoTam iodide, hydriodide
  • HY-154973
    AMPK activator 11
    		Activator
    AMPK activator 11 is an AMP-activated protein kinase (AMPK) activator with nanomolelevel antiproliferation activities against several CRCs. AMPK activator 11 selectively inhibits the RKO xenograft growth along by activating AMPK and upregulating oxidative phosphorylation (OXPHOS) ( mitochondrial metabolism ) and can be used for anti-tumor and metabolic disease research.
    AMPK activator 11
  • HY-Y0624R
    4-Pentenoic acid (Standard)
    4-Pentenoic acid (Standard) is the analytical standard of 4-Pentenoic acid (HY-Y0624). This product is intended for research and analytical applications. 4-Pentenoic acid is a medium-chain unsaturated fatty acid. 4-Pentenoic acid has hypoglycemic and fatty acid oxidation inhibitory activities. 4-Pentenoic acid can affect blood glucose metabolism and energy metabolism through mechanisms such as inhibiting long-chain fatty acid oxidation, reducing gluconeogenesis, and promoting glucose utilization.
    4-Pentenoic acid (Standard)
  • HY-W128525R
    Menadiol (Standard)
    Cloprednol (Standard) is the analytical standard of Cloprednol. This product is intended for research and analytical applications. Cloprednol is an orally active synthetic glucocorticoid. Cloprednol has anti-inflammatory activity, and can be used in the research of asthma.
    Menadiol (Standard)
  • HY-155227S
    ALK/EGFR-IN-1-d5
    		Inhibitor
    ALK/EGFR-IN-1-d5 (Compound (-)-9a) is a deuterated dual-target inhibitor of EGFR and ALK, with an IC50 of 1.08 nM for EGFR and an IC50 of 2.395 nM for ALK. ALK/EGFR-IN-1-d5 inhibits the phosphorylated proteins in the EGFR, ALK, and BRK signaling pathways, blocking the cell cycle, leading to a reduction in mitochondrial membrane potential and cell apoptosis (Apoptosis). ALK/EGFR-IN-1-d5 also significantly inhibits tumor growth in animal models and demonstrates good safety. ALK/EGFR-IN-1-d5 holds promise for research in the field of cancer treatment
    ALK/EGFR-IN-1-d5
  • HY-P10247
    Amyloid precursor C-terminal peptide
    Amyloid precursor C-terminal peptide is cleaved from the C-terminus of Amyloid Precursor Protein (APP). Amyloid precursor C-terminal peptide accumulation causes mitochondrial morphology alteration and basal mitophagy failure, which indicates that amyloid precursor protein C-terminal peptide may correspond to an etiological trigger of Alzheimer’s disease (AD) pathology.
    Amyloid precursor C-terminal peptide
Cat. No. Product Name / Synonyms Application Reactivity