Fact Meets Function

The Precision Peptide Company Inc. Signs Agreement with U.S.-Based 503A Sterile Compounding Pharmacy – Peptides to be 100% Compounded in the United States – TMX Newsfile

The Precision Peptide Company Inc. Signs Agreement with U.S.-Based 503A Sterile Compounding Pharmacy – Peptides to be 100% Compounded in the United States  TMX Newsfile

The Precision Peptide Company Inc. Signs Agreement with U.S.-Based 503A Sterile Compounding Pharmacy – Peptides to be 100% Compounded in the United States – TMX Newsfile Read Post »

The Precision Peptide Company Inc. Signs Agreement with U.S.-Based 503A Sterile Compounding Pharmacy – Peptides to be 100% Compounded in the United States – Yahoo Finance

The Precision Peptide Company Inc. Signs Agreement with U.S.-Based 503A Sterile Compounding Pharmacy – Peptides to be 100% Compounded in the United States  Yahoo Finance

The Precision Peptide Company Inc. Signs Agreement with U.S.-Based 503A Sterile Compounding Pharmacy – Peptides to be 100% Compounded in the United States – Yahoo Finance Read Post »

Lysine-proline-valine peptide attenuates hepatic lipid accumulation through ROS-dependent regulation of the PPARγ pathway in HepG2 cells.

A new in vitro study demonstrates that KPV, one of Annular’s peptide compounds, significantly reduces fat accumulation in liver cells exposed to oleic acid, a model for non-alcoholic fatty liver disease (NAFLD). The research shows KPV works by reducing oxidative stress and regulating key fat-production pathways, specifically targeting the PPAR gamma pathway that controls fatty acid synthesis. At 100 μg/mL concentration, KPV prevented liver cell damage and normalized fat metabolism without toxicity. This provides mechanistic evidence for KPV’s potential therapeutic role in treating hepatic steatosis, the early stage of NAFLD.

Lysine-proline-valine peptide attenuates hepatic lipid accumulation through ROS-dependent regulation of the PPARγ pathway in HepG2 cells. Read Post »

Nicotinamide mononucleotide enhances anti-tumor effect by resetting macrophages toward the inflammatory M1-like phenotype.

NMN supplementation at high doses demonstrated anti-tumor efficacy comparable to PD-1 checkpoint inhibitors in a murine mesothelioma model by reprogramming tumor-associated macrophages toward a pro-inflammatory M1 phenotype rather than enhancing T cell or NK cell responses. This represents a novel immunotherapy mechanism distinct from current checkpoint blockade strategies. The findings suggest NMN may offer an alternative or complementary cancer immunotherapy approach by modulating innate immunity through macrophage phenotype shifting.

Nicotinamide mononucleotide enhances anti-tumor effect by resetting macrophages toward the inflammatory M1-like phenotype. Read Post »

Hepatic Hamp restoration contributes to nicotinamide mononucleotide (NMN)-alleviated hepatic steatosis in chronic alcohol-fed mice.

NMN supplementation restored hepatic NAD+ levels in alcohol-fed mice, which attenuated liver steatosis, inflammation, and oxidative stress through restoration of the Hamp iron-regulation pathway. The mechanism involves C/EBPα-mediated transcriptional control of Hamp expression, linking NAD+ metabolism to iron homeostasis and lipid metabolism. This identifies NMN as a targeted dietary therapeutic for alcohol-associated liver disease (ALD) with a well-characterized molecular pathway, offering practitioners a science-backed rationale for recommending NMN to patients with metabolic liver dysfunction.

Hepatic Hamp restoration contributes to nicotinamide mononucleotide (NMN)-alleviated hepatic steatosis in chronic alcohol-fed mice. Read Post »

Scroll to Top