2. Metabolic Enzyme/Protease
  3. Mitochondrial Metabolism
  4. Mitochondrial respiration-IN-1

Mitochondrial respiration-IN-1 is a mitochondrial respiratory inhibitor. Mitochondrial respiration-IN-1 reduces platelet aggregation, adhesion, and platelet-induced coagulation responses. Mitochondrial respiration-IN-1 induces adaptive glycolysis, decreases mitochondrial membrane potential, selectively reduces ATP production derived from oxidative phosphorylation, and exerts bidirectional regulatory effects on cell proliferation. Mitochondrial respiration-IN-1 activates UPRmt and upregulates the expression of SDHA-1 and MT-CO1. Mitochondrial respiration-IN-1 restores metabolic homeostasis in type 2 diabetic mice. Mitochondrial respiration-IN-1 can be used to investigate diseases mediated by inappropriate platelet activation/aggregation and type 2 diabetes.

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Mitochondrial respiration-IN-1

Mitochondrial respiration-IN-1 Chemical Structure

CAS No. : 1352002-58-4

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Description

Mitochondrial respiration-IN-1 is a mitochondrial respiratory inhibitor. Mitochondrial respiration-IN-1 reduces platelet aggregation, adhesion, and platelet-induced coagulation responses. Mitochondrial respiration-IN-1 induces adaptive glycolysis, decreases mitochondrial membrane potential, selectively reduces ATP production derived from oxidative phosphorylation, and exerts bidirectional regulatory effects on cell proliferation. Mitochondrial respiration-IN-1 activates UPRmt and upregulates the expression of SDHA-1 and MT-CO1. Mitochondrial respiration-IN-1 restores metabolic homeostasis in type 2 diabetic mice. Mitochondrial respiration-IN-1 can be used to investigate diseases mediated by inappropriate platelet activation/aggregation and type 2 diabetes[1][2].

In Vitro

Mitochondrial respiration-IN-1 (Compound 49) (treated at 0°C for 2 min) irreversibly inhibits mitochondrial respiration in isolated tilapia liver mitochondria, and after washing and resuspension, its respiratory rate cannot recover to more than 75% of the baseline level[1].
Mitochondrial respiration-IN-1 (Compound 1) (25-200 μM; 24 h) acts as a mild dose-dependent inhibitor of mitochondrial respiration in HepG2 cells, reducing spare respiratory capacity by 30% and suppressing maximal respiration under the treatment condition of 200 μM for 24 h[2].
Mitochondrial respiration-IN-1 (25-200 μM; 90 min) reduces the mitochondrial membrane potential of HepG2 cells in a dose-dependent manner. After treatment with 200 μM for 90 min, the proportion of cells with high ΔΨm decreases by 55%[2].
Mitochondrial respiration-IN-1 (25-100 μM; 90 min) selectively inhibits mitochondrial oxidative phosphorylation-mediated ATP production in HepG2 cells in a dose-dependent manner, with no effect on ATP production via the glycolytic pathway[2].
Mitochondrial respiration-IN-1 (25-100 μM; 0-30 h) exerts reversible mitochondrial inhibitory toxicity on HepG2 cells at concentrations of 25 μM and 50 μM, but induces irreversible, progressively worsening toxicity after treatment at 100 μM for 30 h[2].
Mitochondrial respiration-IN-1 (25-200 μM; up to 120 h) exerts a biphasic effect on the proliferation of HepG2 cells: after 72 h of treatment, it promotes cell growth at the concentration of 25 μM, while strongly inhibits cell proliferation at 200 μM[2].
Mitochondrial respiration-IN-1 (12.5-200 μM; 24 h) induces adaptive glycolysis in HepG2 cells at concentrations ranging from 12.5 μM to 100 μM, but causes glycolysis collapse and reduced mitochondrial acidification levels after 24 h treatment at 200 μM[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Mitochondrial respiration-IN-1 Related Antibodies

Cell Proliferation Assay[2]

Cell Line: HepG2
Concentration: 0, 25, 50, 100, 200 μM
Incubation Time: up to 120 h
Result: Elicited a concentration-dependent biphasic effect on HepG2 proliferation.
Stimulated cell growth at 25 μM, with significantly higher cell index than control at 72 h.
Had no significant effect on proliferation at 50 μM.
Inhibited proliferation at 100 μM.
Strongly suppressed growth at 200 μM .
In Vivo

Mitochondrial respiration-IN-1 (25 mg/kg; i.p.; three times weekly; 2 months) improves glucose homeostasis, insulin sensitivity, and lipid metabolism, and reduces hepatic steatosis in diet-induced insulin-resistant mice, with greater efficacy than metformin and no detectable toxicity[2].
Mitochondrial respiration-IN-1 (25 mg/kg; i.p.; single dose) induces systemic mitokine (FGF21) expression in healthy mice without acute hypothermia[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: C57BL/6J (male, 6 weeks old at study start, diet-induced insulin resistance: 10 weeks high-fat diet + 75 mg/kg Streptozotocin (HY-13753) injection)[2]
Dosage: 25 mg/kg
Administration: i.p.; three times weekly; 2 months
Result: Reduced non-fasting blood glucose to levels lower than metformin-treated mice.
Improved glucose tolerance, with lower blood glucose levels at all time points post-glucose injection compared to saline-treated HFD-IR mice.
Reduced fasting blood glucose from ~18 mM to ~13 mM, a greater reduction than metformin (~14 mM).
Improved insulin sensitivity, with 120 min post-insulin blood glucose reduced from ~28 mM to ~18 mM, a greater improvement than metformin (~23 mM).
Increased VO2 and VCO2 levels (day and night) compared to saline-treated HFD-IR mice, with a higher respiratory exchange rate indicating enhanced glucose utilization.
Reduced circulating non-esterified fatty acids from ~1600 mmol/L to ~800 mmol/L, triglycerides from ~6 mmol/L to ~0.5 mmol/L, and LDL from ~1.3 mmol/L to ~0.8 mmol/L, and increased HDL from ~3.2 mmol/L to ~3.8 mmol/L compared to saline-treated HFD-IR mice.
Reduced liver weight from ~1.8 g to ~1.5 g, with macroscopic and histological evidence of reduced steatosis.
Upregulated oxidative phosphorylation, fatty acid metabolism, AMPK signaling, and PPAR signaling pathways in liver and iWAT, with specific upregulation of respiratory chain complex IV genes in both tissues.
Showed no significant toxicity: no mortality, preserved organ weights, unchanged rectal temperature, normal cardiac ultrasonography, and unaltered liver (ALT, AST) and kidney (BUN) function markers.
Animal Model: C57BL/6J (male, 8 weeks old)[2]
Dosage: 25 mg/kg
Administration: i.p.; single dose
Result: Increased hepatic FGF21 mRNA levels ~3.5-fold compared to saline control.
Increased blood FGF21 mRNA levels ~4-fold compared to saline control.
Showed no significant drop in rectal temperature 1 h post-injection.
Molecular Weight

526.42

Formula

C26H25BrNO2PS
CAS No.
SMILES

O=C(OCCC1=C(C)N=CS1)C[P+](C2=CC=CC=C2)(C3=CC=CC=C3)C4=CC=CC=C4.[Br-]
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.
Solvent & Solubility
In Vitro: 

DMSO : 66.67 mg/mL (126.65 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)

Preparing
Stock Solutions
Concentration Solvent Mass 1 mg 5 mg 10 mg
1 mM 1.8996 mL 9.4981 mL 18.9962 mL
5 mM 0.3799 mL 1.8996 mL 3.7992 mL
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In Vivo:

Select the appropriate dissolution method based on your experimental animal and administration route.

For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for in vivo experiments, it is recommended to prepare freshly and use it on the same day.
The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.

  • Protocol 1

    Add each solvent one by one:  10% DMSO    40% PEG300    5% Tween-80    45% Saline

    Solubility: 5 mg/mL (9.50 mM); Suspended solution; Need ultrasonic

    This protocol yields a suspended solution of 5 mg/mL. Suspended solution can be used for oral and intraperitoneal injection.

    Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (50.0 mg/mL) to 400 μL PEG300, and mix evenly; then add 50 μL Tween-80 and mix evenly; then add 450 μL Saline to adjust the volume to 1 mL.

    Preparation of Saline: Dissolve 0.9 g sodium chloride in ddH₂O and dilute to 100 mL to obtain a clear Saline solution.
  • Protocol 2

    Add each solvent one by one:  10% DMSO    90% (20% SBE-β-CD in Saline)

    Solubility: ≥ 5 mg/mL (9.50 mM); Clear solution

    This protocol yields a clear solution of ≥ 5 mg/mL (saturation unknown).

    Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (50.0 mg/mL) to 900 μL 20% SBE-β-CD in Saline, and mix evenly.

    Preparation of 20% SBE-β-CD in Saline (4°C, storage for one week): 2 g SBE-β-CD powder is dissolved in 10 mL Saline, completely dissolve until clear.
In Vivo Dissolution Calculator
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Method for preparing stock solution: mg drug dissolved in μL  DMSO (Stock solution concentration: mg/mL).
The concentration of the stock solution you require exceeds the measured solubility. The following solution is for reference only. If necessary, please contact MedChemExpress (MCE).
Method for preparing in vivo working solution for animal experiments: Take μL DMSO stock solution, add μL . μL , mix evenly, next add μL Tween 80, mix evenly, then add μL Saline.
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Please ensure that the stock solution in the first step is dissolved to a clear state, and add co-solvents in sequence. You can use ultrasonic heating (ultrasonic cleaner, recommended frequency 20-40 kHz), vortexing, etc. to assist dissolution.
Purity & Documentation
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Complete Stock Solution Preparation Table

Optional Solvent Concentration Solvent Mass 1 mg 5 mg 10 mg 25 mg
DMSO 1 mM 1.8996 mL 9.4981 mL 18.9962 mL 47.4906 mL
5 mM 0.3799 mL 1.8996 mL 3.7992 mL 9.4981 mL
10 mM 0.1900 mL 0.9498 mL 1.8996 mL 4.7491 mL
15 mM 0.1266 mL 0.6332 mL 1.2664 mL 3.1660 mL
20 mM 0.0950 mL 0.4749 mL 0.9498 mL 2.3745 mL
25 mM 0.0760 mL 0.3799 mL 0.7598 mL 1.8996 mL
30 mM 0.0633 mL 0.3166 mL 0.6332 mL 1.5830 mL
40 mM 0.0475 mL 0.2375 mL 0.4749 mL 1.1873 mL
50 mM 0.0380 mL 0.1900 mL 0.3799 mL 0.9498 mL
60 mM 0.0317 mL 0.1583 mL 0.3166 mL 0.7915 mL
80 mM 0.0237 mL 0.1187 mL 0.2375 mL 0.5936 mL
100 mM 0.0190 mL 0.0950 mL 0.1900 mL 0.4749 mL
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  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

Mitochondrial respiration-IN-11352002-58-4Mitochondrial Metabolismmitochondrial respiratory chain Complexes IVtilapia liver mitochondriaMT-CO1plateletSDHA-1cytochrome c oxidasemitochondrial respiratory chain Complexes IIIHepG2 cellsmitokineUPRmtInhibitorinhibitorinhibit

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