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Cardiolipin solution from bovine heart

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For Research Use Only | Not For Clinical Use
CATIAR4247129
MDL NumberMFCD00071040
EC Number200-578-6
1

Increase in Water Permeability of Negatively Charged Liposomal Membrane by Local Anesthetics

T Shimooka, S Seto, H Terada

Chem Pharm Bull (Tokyo). 1992 Jul;40(7):1880-2.

PMID: 1394708

1

Interactions Between Phospholipids and NADH:ubiquinone Oxidoreductase (Complex I) From Bovine Mitochondria

Mark S Sharpley, Richard J Shannon, Federica Draghi, Judy Hirst

Biochemistry. 2006 Jan 10;45(1):241-8.

PMID: 16388600

1

Mechanism of Activation of Cytochrome C Peroxidase Activity by Cardiolipin

Yu A Vladimirov, E V Proskurnina, D Yu Izmailov, A A Novikov, A V Brusnichkin, A N Osipov, V E Kagan

Biochemistry (Mosc). 2006 Sep;71(9):989-97.

PMID: 17009953

1

Significant Stabilization of the Phosphatidylcholine Bilayer Structure by Incorporation of Small Amounts of Cardiolipin

A Shibata, K Ikawa, T Shimooka, H Terada

Biochim Biophys Acta. 1994 Jun 1;1192(1):71-8.

PMID: 8204653

1

Site of Action of the Local Anesthetic Tetracaine in a Phosphatidylcholine Bilayer With Incorporated Cardiolipin

A Shibata, K Ikawa, H Terada

Biophys J. 1995 Aug;69(2):470-7.

PMID: 8527661

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CATSizeDescriptionPrice
IAR4247129-1 10MG, 25MG, 100MG, 500MG 4.7-5.3 mg/mL in ethanol, ≥97% (TLC) Inquiry
IAR4247129-2 50MG, 100MG, 250MG, 5000MG, 1G 4.7-5.3 mg/mL in ethanol, ≥97% (TLC), Suitable for manufacturing of diagnostic kits and reagents Inquiry
Case Study

Cardiolipin Used for the Modulation of Potassium Channel Activity in Acidic Membrane Environments

Iwamoto, M., Morito, M., Oiki, S., Nishitani, Y., Yamamoto, D., & Matsumori, N. (2023). Iscience, 26(12).

Cardiolipin (CL), a dianionic phospholipid predominantly localized in bacterial and mitochondrial membranes, plays a pivotal role in modulating membrane protein function. In a recent study focused on the potassium channel KcsA from Streptomyces, CL was shown to exhibit remarkably high affinity for the channel, particularly under acidic conditions (pH 4.0), mimicking the channel's activated state.
Using a surface plasmon resonance (SPR)-based assay, researchers found that CL binds to both the lipid-sensing N-terminal M0 helix and an additional site within the transmembrane domain, suggesting multiple, functionally relevant interaction points. This contrasts with monoanionic lipids, such as phosphatidic acid (PA), which primarily associate with the M0 helix and show lower affinity. Notably, the dissociation constant (KD) for CL-KcsA interaction at pH 4.0 is in the nanomolar range (KA ≈ 10⁹), with a very low off-rate (koff), confirming strong and specific binding under acidic conditions.
Single-channel electrophysiological recordings further revealed that CL significantly enhances KcsA channel opening in an M0-independent manner, supporting a distinct allosteric mechanism of channel modulation.
These findings demonstrate that cardiolipin is used for the modulation of potassium channel activity through high-affinity, pH-dependent interactions, and highlight its essential role in regulating ion channel function in native bacterial membranes.

Cardiolipin Used for the Modulation of Vesicle Morphology and Lamellarity in Lipid Membrane Models

Piccinini, Alice, et al. Journal of Colloid and Interface Science 669 (2024): 844-855.

Cardiolipin (CL), a tetra-acylated phospholipid abundant in bacterial and mitochondrial membranes, plays a crucial role in modulating membrane structure and vesicle morphology. In this study, small-angle X-ray scattering (SAXS) and neutron scattering (SANS) techniques were employed to investigate how different types of cardiolipin-CL14:0, CL18:1, and CL18:2-affect lamellarity and curvature in lipid vesicles composed of phosphatidylcholine (PC) and phosphatidylethanolamine (PE) mixtures.
Measurements were performed in phosphate-buffered saline (PBS) at 37 °C to reflect physiological conditions. Even low concentrations of cardiolipin (as low as 2.5 wt%) led to significant reductions in inter-membrane correlations and induced membrane perturbations, especially when the acyl chains of CL and PC/PE were of matching length and saturation. These conditions favored the formation of predominantly unilamellar vesicles (ULVs), while mismatched chains or hypertonic environments promoted flattened or multilamellar structures.
SAXS data indicated that vesicles without cardiolipin exhibited stacked lamellar phases, as seen by sharp Bragg reflections. The introduction of cardiolipin disrupted this stacking in a concentration- and structure-dependent manner, emphasizing its critical role in lipid organization.
This product is used for the modulation of vesicle morphology and lamellarity in phospholipid membrane systems, offering key insights into membrane biophysics relevant to both cellular biology and drug delivery research.

Cardiolipin Used for Regulating Mitochondrial Stress Response and Pyroptosis in Retinal Epithelial Cells

Davidescu, M., Mezzasoma, L., Fettucciari, K., Pascucci, L., Pariano, M., Di Michele, A., ... & Macchioni, L. (2023). Biochimica et Biophysica Acta (BBA)-Molecular Cell Research, 1870(8), 119554.

Cardiolipin, a mitochondria-specific phospholipid, plays a central role in regulating cellular fate under oxidative stress conditions. In a study using ARPE-19 cells as a model of retinal pigmented epithelium, cardiolipin was found to mediate critical steps in the cellular response to hydroquinone-an oxidative toxicant found in cigarette smoke.
Hydroquinone exposure induced early mitochondrial dysfunction, characterized by elevated mitochondrial reactive oxygen species (ROS), decreased membrane potential, and increased oxygen consumption, all preceding measurable loss in ATP. Despite these impairments, cell viability was initially maintained through the activation of protective mitophagy.
A key event was the hydroquinone-induced translocation of cardiolipin to the outer mitochondrial membrane, where it acted as an "eat-me" signal by recruiting LC3, thereby facilitating mitophagosome formation. However, prolonged exposure led to a pathological shift: cardiolipin acted as a trigger for pyroptosis by activating caspase-1 and gasdermin-D, culminating in inflammatory cell death. Importantly, cardiolipin-specific antioxidants mitigated these effects, confirming its central regulatory role.
This product is used for regulating mitochondrial stress response and pyroptotic signaling in oxidative stress-induced retinal damage. These findings underscore cardiolipin's dual function as both a mediator of mitochondrial quality control and a trigger for programmed cell death, positioning it as a promising therapeutic target for oxidative stress-related retinal diseases.

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