Weight loss in rhesus monkeys and mice has been caused by the peptidomimetic chemical Adipotide, which has pro-apoptotic characteristics. CKGGRAKDC-GG-D is its alphanumeric code (KLAKLAK). According to research, apoptosis of the white adipose tissue-supplying blood vessels is thought to be the mechanism by which it works. It causes the fat cells to lose their blood supply since the arteries that carry it are atrophying and ultimately dying. Consequently, fat cells suffer ischemia damage, which is caused by a reduction in blood flow and oxygen delivery. Fat cells die due to apoptosis, which is a kind of cell death that cannot be reversed.

Adipotide’s stereochemical structure allows it to attach to two particular receptors only present in blood arteries supplying white adipose tissue, according to molecular research. These receptors are ANXA-2 and prohibitin. Adipotide has no impact on brown adipose tissue because of the tissue specificity of these receptors. Hence it does not influence adaptive brown fat thermogenesis. In infants, brown fat thermogenesis is particularly important since their body surface area/volume ratio promotes high rates of heat loss, making heat conservation difficult. A person’s body produces white adipose tissue only if they consume more energy than they need.


Excess adipose tissue mass is the cause of obesity. According to research, the white adipose tissue that accumulates in the body due to being overweight is the primary culprit. Since an increase in weight might be caused by a rise in lean body mass rather than an increase in adiposity, an increase in weight does not always correspond to obesity. Morbidity and mortality rates rise in the presence of obesity. The BMI (Body Mass Index), anthropometry (using skinfold thickness), and densitometry are now used to measure obesity. Obesity is defined as a BMI of 30 or above. Increased adiposity puts a person at risk for many health problems, including high blood pressure, high cholesterol, metabolic syndrome, non-insulin-dependent diabetes mellitus (NIDDM), stroke, heart attack, and cancer. The morbidity rate is affected by adiposity distribution; for example, abdominal adiposity is more dangerous than adiposity in the buttocks and lower limbs. Their waist-to-hip ratio determines their risk of developing the disorders listed above. Fatty tissue in the abdomen has higher lipolytic activity than adipose tissue in the lower limbs, linked to an increased risk of death and illness.

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It is challenging to translate anti-obesity medicines produced in rodents into medications that can be provided to people because of the biological differences between rodents and primates. If the people investigated were also primate family members, these issues would be alleviated. Weight loss and improved insulin resistance were the results of research done on obese monkeys in 2011. Science Translational Medicine reported the study’s results. A ligand-directed peptidomimetic was tested in obese monkeys in this work. Adipotide, the peptidomimetic sequence for the ligand-directed peptidomimetic, was CKGGRAKDC-GG-D(KLAKLAK). Adipotide was shown to cause apoptosis in the white adipose tissue vasculature, leading to weight reduction in the monkeys and better insulin function. MRI (Magnetic resonance imaging) and DEXA (Dexa scan) verified the reduction in white adipose tissue mass (dual-energy x-ray absorptiometry). The kidney function of the monkeys was also improved as a result of the research. Adipotide was shown to be a prototype for anti-obesity peptides in this investigation. Purchase Adipotide FTPP peptide if you are a scientist interested in further researching this compound.