It's currently in a Phase 1 trial, see here. Prohibitin Targeting Peptide 1 = Adipotide.

Phase 1 trial means that "researchers test an experimental drug or treatment in a small group of people (20-80) for the first time to evaluate its safety, determine a safe dosage range, and identify side effects", so it's designed for establishing safety only (although secondary data may be gathered).

Here's the press release from the substance's owner, Arrowhead. Excerpt:

Multiple independent [animal!] studies with Adipotide have demonstrated that obese rodents lose up to 30% of their body weight after only 28 days of treatment while lean animals show no weight loss. Studies have also shown that obese animals undergo rapid improvement in pro-diabetic metabolic markers, including significantly improved insulin sensitivity, improved glucose tolerance, and a reduction in serum triglycerides after only 2-3 days of treatment. Adipotide has been further studied in non-human primates, and it has been reported that after 28 days of treatment obese rhesus monkeys lost an average of 11% of their body weight, experienced a reduction in body mass index and abdominal circumference, and showed marked improvements in insulin resistance, a marker for type II diabetes. These data were published in the peer-reviewed journal Science Translational Medicine in November 2011 (Sci Trans Med 3, 108-112 (2011) DOI: 10.1126/scitraslmed.3002621).

However, that phase 1 trial is the only study using the substance with humans. Just that study will run until May 2016, and it's using prostate cancer patients. It'll be a while ...

Edit: An excerpt from a critical comment about the cited paper, published by the same journal:

The authors of the study conclude that their findings in primates establish adipotide as a prototype for a new class of candidate drugs that may be useful for treating obesity in humans. The data presented in their paper (Fig. 5C and fig. S3), however, could instead reflect a reduction in food intake induced directly by adipotide that resulted in body weight reduction. (...) This strong reduction in food intake in the absence of an increase in energy expenditure is more than sufficient to explain the reduction in white adipose tissue and body weight reported in this study. The fact that the reduction in food intake lasted at least 1 week after cessation of adipotide treatment suggests that there may be a toxic effect of adipotide.

... and the response by the authors of the original paper:

(...) an independent report that carefully assessed the effects of adipotide on obese rodents unequivocally concluded that the observed decrease in food intake was not the result of nonspecific visceral illness. (...) The primary event appears to be ligand-directed vascular targeting with subsequent peripheral remodeling of white adipose tissue and an increase in peripheral metabolism. Another potential mechanism, a hypothalamic feedback loop, has been (...) empirically demonstrated, but the central molecular signal remains to be identified. Several recent reports indicate that mechanisms of satiety and satiation are influenced by many factors. Some of these factors could be initiated by the targeted destruction of white adipose tissue followed by a consequent increase in peripheral metabolism and a decrease in food intake. Most recently, a study has established that adipotide improves glucose tolerance independent of body weight and food consumption in obese mice, further supporting our proposed mechanism for the observed effects of adipotide.