Design and implication of a breast cancer-targeted drug delivery system utilizing the Kisspeptin/GPR54 system.

Kisspeptins function as endogenous ligands for the G protein-coupled receptor GPR54. While the primary role of the Kisspeptin/GPR54 signaling pathway pertains to reproduction, several studies have shown that GPR54 is highly expressed in breast cancer, and we further confirmed this result that GPR54 expression is significantly upregulated in breast cancer cells. Based on this finding, we developed a liposomal drug delivery system utilizing the Kisspeptin/GPR54 system to treat breast cancer after confirming the safety of Kp-10-228.

Orally administered MOTS-c analogue ameliorates dextran sulfate sodium-induced colitis by inhibiting inflammation and apoptosis.

Inflammatory bowel disease (IBD) is a chronic and relapsing inflammatory disorder of the gastrointestinal tract (GI). Currently, the treatment options for IBD are limited. It has been reported that a novel bioactive mitochondrial-derived peptide (MOTS-c) encoded in the mitochondrial 12S rRNA, suppresses inflammatory response by enhancing the phagocytosis of macrophages.

Peripheral Administration of a Cell-Penetrating MOTS-c Analogue Enhances Memory and Attenuates Aβ- or LPS-Induced Memory Impairment through Inhibiting Neuroinflammation.

MOTS-c is a 16-amino acid mitochondrial derivative peptide reported to be involved in regulating insulin and metabolic homeostasis via the AMP activated protein kinase (AMPK). AMPK agonist AICAR has been reported to improve cognition. Previous reports also pointed out that MOTS-c may be effective as a therapeutic option toward the prevention of the aging processes.

Intranasal MMI-0100 Attenuates Aβ- and LPS-Induced Neuroinflammation and Memory Impairments via the MK2 Signaling Pathway.

Accumulating evidence suggests inhibiting neuroinflammation as a potential target in therapeutic or preventive strategies for Alzheimer's disease (AD). MAPK-activated protein kinase II (MK2), downstream kinase of p38 mitogen activated protein kinase (MAPK) p38 MAPK, was unveiled as a promising option for the treatment of AD. Increasing evidence points at MK2 as involved in neuroinflammatory responses.