Anti-INS monoclonal antibody, clone 4B7

Insulin is a polypeptide hormone primarily secreted by pancreatic beta cells, regulating glucose storage and reduction in the liver, muscle, and adipose tissues. When tissues exhibit a reduced response to normal insulin levels, insulin resistance (IR) occurs. IR is considered a heterogeneous disease that leads to elevated blood glucose levels, with cells unable to access glycogen converted from glucose for normal energy storage, instead relying on fat storage for energy supply, which leads to the onset of type 2 diabetes (T2DM). This chronic condition causes patients to experience continuous weight loss, emaciation, ketoacidosis, and ultimately coma and death. A range of serious health complications, such as neurological damage often accompanies diabetes. T2DM patients cannot effectively utilize endogenous insulin, thus requiring exogenous insulin to manage their condition. The levels and mechanisms of insulin, insulin therapy, and insulin resistance remain hot topics in contemporary research.

A century ago, humans began using insulin to treat diabetes. Even in modern times, although we know it cannot cure diabetes, it remains the most widespread and fundamental treatment method for diabetes. Current T2DM medications on the market are relatively ineffective, often alleviating hyperglycemia by stimulating insulin secretion or directly supplementing with exogenous insulin. These methods necessitate frequent short-term injections and exogenous insulin still fails to mimic the characteristics of physiological insulin, resulting in generally poor overall glycemic control. Therefore, avoiding subcutaneous administration and developing exogenous insulin that better mimics physiological insulin characteristics are key focuses of current insulin-related research. In recent years, new drugs requiring only weekly administration and oral insulin are undergoing clinical trials, with their efficacy and potential side effects yet to be fully confirmed.

Figure 1. Classic insulin signaling pathway (Source: Rahman MS, et al., 2021)

The molecular mechanisms related to insulin resistance remain to be elucidated. Numerous animal and epidemiological studies have confirmed that ectopic lipid accumulation in hepatocytes and reduced lipid oxidation in skeletal muscle, involving several lipid metabolites including diacylglycerol (DAG), lysophosphatidic acid (LPA), ceramide, and acylcarnitine, may be key mechanisms of hepatic and systemic insulin resistance. Thus, developing insulin-resistance drugs could focus on inhibiting hepatic lipid synthesis. Additionally, skeletal muscle has received insufficient attention in previous studies, as it constitutes over one-third of body weight and is responsible for processing 70%-80% of glucose following insulin stimulation. Therefore, increasing fat oxidation and skeletal muscle mass is considered a potential strategy to reduce lipid accumulation within muscle cells and ultimately improve insulin sensitivity.

Anti-Insulin monoclonal antibody, clone 4B7
Insulin antibody, clone 4B7
Insulin monoclonal antibody, clone 4B7
Anti-Insulin MAb, clone 4B7
Anti-INS MAb, clone 4B7
Clone 4B7 Anti-Insulin monoclonal antibody