mitochondrial phospholipid

Imeglimin hydrochloride (EMD 387008 hydrochloride) is an oral hypoglycemic agent. Imeglimin improves insulin sensitivity, inhibits the production of reactive oxygen species, increases mitochondrial DNA, and improves mitochondrial function.

KIT-13 is an orally active acetal phospholipid derivative that effectively inhibits neuroinflammation and addresses mitochondrial DNA leakage issues associated with Mecp2 deficiency. It significantly alleviates neurological symptoms and prolongs lifespan in Rett Syndrome (RTT) model mice. KIT-13 is valuable for research in RTT and other neuroinflammation-related conditions.

TBPH exacerbates liver steatosis, inflammation, and fibrosis in non-alcoholic steatohepatitis (NASH) mouse models. It induces phospholipid metabolism disorders, reducing cardiolipin (CL) and phosphatidylserine (PS) levels. TBPH impairs endoplasmic reticulum-mitochondria (ER-Mito) contact, leading to mitochondrial dysfunction. Additionally, TBPH causes lung injury through mitochondrial-derived ds-DNA-mediated inflammatory responses. TBPH is utilized to study the role of MFN2-mediated ER-Mito contact in lipid metabolism homeostasis.

Epsilon-V1-2 has been extensively investigated for its function as a PKC epsilon (PKCε) inhibitor. Epsilon-V1-2 has been widely applied in studies addressing ovarian aging, apoptosis in human granulosa cells, cerebral ischemia-reperfusion injury, brain development, hepatocyte insulin signaling, and neuronal cell death under ischemic conditions. Epsilon-V1-2 has been shown to effectively reduce PKCε activity, thereby enabling detailed exploration of regulatory pathways involving mitochondrial dynamics, calcium overload, AKT activation, brain atrophy, insulin resistance, and ferroptosis. Epsilon-V1-2 demonstrates notable therapeutic relevance in models of stroke, SHORT syndrome, hepatic steatosis, and brain injury, supporting its continued evaluation as a potential pharmacological agent across multiple disease contexts.

CAY10726 is an arylurea fatty acid. It decreases ATP production by 28% in MDA-MB-231 breast cancer cells when used at a concentration of 10 μM. CAY10726 decreases proliferation and initiates apoptosis in MDA-MB-231 cells via depletion of the phospholipid cardiolipin and its precursor phosphatidylglycerol from the mitochondrial membrane. In vivo, CAY10726 (2.5-40 mg/kg) reduces tumor volume and increases tumor cell apoptosis in a mouse MDA-MB-231 breast cancer xenograft model in a dose-dependent manner.

Phosphatidic acid is a phospholipid and an intermediate in glycerolipid biosynthesis. It is a transient intermediate in the synthesis of various phospholipid species that is synthesized de novo in cells via multiple routes, including the glycerol-3 phosphate and dihydroxyacetone phosphate pathways, enzymatic conversion of phosphatidylcholine by phospholipase D, and acetylation of lysophosphatidic acid by lysoPA-acyltransferase, among others. It has roles in shaping cellular membranes, cellular signaling, vesicle fission and fusion, as well as mitochondrial division and fusion. It stimulates respiratory burst in neutrophils independent of diacylglycerol and activates monoacylglycerol acyltransferase, phospholipase C (PLC), Ras, and phosphatidylinositol 4-phosphate (PIP4) kinase in several cell lines. Phosphatidic acids (egg) is a mixture of phosphatidic acids isolated from chicken egg with fatty acids of variable chain lengths.

L-Cytidine, an L-configurational form of Cytidine, is a pyrimidine nucleoside and a component of RNA. It influences the glial glutamate cycle, brain phospholipid metabolism, catecholamine synthesis, and mitochondrial function [1] [2].

Cardiolipin (Heart, Bovine) sodium is a phospholipid found in mitochondria and is involved in mitochondrial structure and function.Cardiolipin (Heart, Bovine) sodium is used in the study of neurological, cardiovascular, and metabolic diseases.

1-Stearoyl-2-arachidonoyl-sn-glycero-3-phosphorylethanolamine (SAPE) is a natural phospholipid found in mitochondrial inner membranes, involved in lipid signaling.