Goal
Best-studied peptides for weight loss
Ranked by the strongest evidence rung each compound holds, with what the study measured beside it. 48 were checked; 29 produced a graded row.
Last updated
48 compounds were read against these 4 conditions; 29 produced a graded row. The other 19 are named further down.
The ranking, and the key it uses
Ordered by the best rung the compound holds anywhere in this goal; then by what that study measured; then by how many graded rows it holds here, as a tie-break only; then by name. There is no blended score — one number mixing the rung and what was measured would invent a third scale nothing was graded against. Every rung links to the rubric that assigned it.
Reading the strip
1 human RCT2 human observational3 human case series4 animal in vivo5 in vitro6 theoretical7 computational
A filled cell means at least one graded row at that rung. Its colour is what the strongest such study measured: direct outcome · surrogate marker · mechanistic only. An outlined cell means no row at that rung.
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Cagrilintide
human RCT · direct outcome · 2 graded rows across 2 of 4 conditions
2 graded rows, 1 source
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Obesity
human RCT Direct outcome In registered trials
- Who was studied
- adults with obesity, or overweight with at least one weight-related comorbidity; n=706, 26 weeks
A dose-finding phase 2 trial randomised participants to five cagrilintide doses, placebo, or liraglutide 3.0 mg, and measured change in body weight over 26 weeks. Cagrilintide is not approved anywhere, alone or in combination.
Source PubMed 1 primary source read for this row
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Weight management
human RCT Direct outcome In registered trials
- Who was studied
- adults with obesity, or overweight with at least one weight-related comorbidity; n=706, 26 weeks
A dose-finding phase 2 trial randomised participants to five cagrilintide doses, placebo, or liraglutide 3.0 mg, and measured change in body weight over 26 weeks. The evidence comes from a clinical population enrolled for obesity or overweight with a comorbidity, not from people in the healthy range managing their weight. Cagrilintide is not approved anywhere, alone or in combination.
Source PubMed 1 primary source read for this row
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Dulaglutide
human RCT · direct outcome · 2 graded rows across 2 of 4 conditions
2 graded rows, 1 source
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Obesity
human RCT Direct outcome Not approved for this condition
- Who was studied
- adults with type 2 diabetes inadequately controlled on metformin; n=1842, 52 weeks; obesity was not an enrolment criterion
AWARD-11 randomised participants to dulaglutide 1.5, 3.0 or 4.5 mg and measured change in body weight as a secondary endpoint over 52 weeks; the primary endpoint was HbA1c. Enrolment was by glycaemic control, not by BMI, and no trial of dulaglutide in people without diabetes selected for obesity is on file.
Source PubMed 1 primary source read for this row
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Weight management
human RCT Direct outcome Not approved for this condition
- Who was studied
- adults with type 2 diabetes inadequately controlled on metformin; n=1842, 52 weeks; neither BMI nor weight was an enrolment criterion
AWARD-11 measured change in body weight only as a secondary endpoint over 52 weeks; the primary endpoint was HbA1c and enrolment was by glycaemic control. The evidence comes from a diabetes population, not from healthy people managing weight, and no trial of dulaglutide selected for weight in people without diabetes is on file. Dulaglutide has no weight-management approval anywhere.
Source PubMed 1 primary source read for this row
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Exenatide
human RCT · direct outcome · 2 graded rows across 2 of 4 conditions
2 graded rows, 1 source
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Obesity
human RCT Direct outcome Not approved for this condition
- Who was studied
- obese women without diabetes, mean BMI 33.1, n=41, 35-week crossover with two 16-week treatment periods
A randomised double-blind placebo-controlled crossover study measured body weight change in obese women without diabetes; mean loss was 2.49 kg on exenatide against a 0.43 kg gain on placebo. Men were not enrolled, and no phase 3 obesity programme for exenatide is on file.
Source PubMed 1 primary source read for this row
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Weight management
human RCT Direct outcome Not approved for this condition
- Who was studied
- obese women without diabetes, mean BMI 33.1, n=41, 35-week crossover with two 16-week treatment periods
A randomised double-blind placebo-controlled crossover study measured body weight change; mean loss was 2.49 kg on exenatide against a 0.43 kg gain on placebo. The evidence comes from obese women only — a clinical population, not people in the healthy range managing their weight — men were not enrolled, and no phase 3 weight programme for exenatide is on file.
Source PubMed 1 primary source read for this row
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GHRP-2
human RCT · direct outcome · 2 graded rows across 2 of 4 conditions
2 graded rows, 1 source
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Obesity
human RCT Direct outcome Not approved for this condition
- Who was studied
- 9 obese and 10 lean healthy adults within the same crossover study; single-session infusion, no chronic dosing
The same crossover study asked specifically whether obese participants still respond, and they did: the increase in food intake and in growth hormone was present in obese and lean participants alike and rose with dose. That is a finding about preserved ghrelin-receptor responsiveness in obesity, not a treatment result — no obesity trial of GHRP-2 exists, and no study on file measured weight, waist or fat mass in obese participants over any period. Rung set from the study's own design wording, "double-blind randomized".
Source PubMed 1 primary source read for this row
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Excess food intake
human RCT Direct outcome Not approved for this condition
- Who was studied
- 19 healthy weight-stable adults, 10 lean and 9 obese; subcutaneous infusion at 1 microgram/kg/hour, 0.1 microgram/kg/hour or placebo for 270 minutes across three visits, with an ad libitum buffet lunch as the endpoint
The direction of this result is towards more eating, not less. GHRP-2 raised ad libitum food intake by 10.2 per cent at the low dose and 33.5 per cent at the high dose against placebo, and obesity status did not blunt the response. Appetite ratings before the meal rose; fullness after the meal did not differ. A compound recorded here against excess food intake because it was measured against that endpoint and moved it upward; nothing in the record supports it as a treatment for the condition. The exposure was a single infusion in a laboratory meal paradigm, so no weight outcome over time is on file. Rung set from the study's own design wording, "double-blind randomized".
Source PubMed 1 primary source read for this row
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2 graded rows, 2 sources
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Obesity
human RCT Direct outcome Not approved for this condition
- Who was studied
- adults across 9 randomised controlled trials, n=911 pooled; trial durations varied and the pooled effect fell as duration lengthened
A systematic review and meta-analysis of randomised trials measured body weight and BMI, finding a pooled mean difference of -1.33 kg (95% CI -2.09 to -0.57) against control. Meta-regression showed the magnitude decreased significantly over time, and the pooled trials are far smaller and shorter than the incretin obesity programmes.
Source PubMed 1 primary source read for this row
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Fat loss
human RCT Direct outcome Not approved for this condition
- Who was studied
- adults across 37 randomised controlled trials, 2292 participants pooled; effect reported as confined to adults with overweight or obesity; trial durations vary
A meta-analysis of 37 randomised controlled trials found pooled reductions of 1.21 kg in body weight, 0.24 kg/m2 in BMI and 2.08 kg in fat mass, with no significant change in body fat percent or waist circumference. Fat mass was measured, so this is not scale weight alone, but the unchanged body fat percent means the data do not establish a shift in composition. Restricting to high-quality trials confirmed only the body-weight effect, and the reported benefit was in overweight and obese participants.
Source PubMed 1 primary source read for this row
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Pramlintide
human RCT · direct outcome · 2 graded rows across 2 of 4 conditions
2 graded rows, 1 source
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Obesity
human RCT Direct outcome Not approved for this condition
- Who was studied
- obese adults not treated with insulin, mean BMI 37.8, 80 percent female; n=204, 16 weeks
A phase 2 randomised placebo-controlled dose-escalation study measured body weight and waist circumference over 16 weeks, with a placebo-corrected weight reduction of 3.7 percent. Pramlintide's approval is as a mealtime insulin adjunct in diabetes; no obesity approval is on file and the obesity programme did not proceed to registration.
Source PubMed 1 primary source read for this row
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Weight management
human RCT Direct outcome Not approved for this condition
- Who was studied
- obese adults not treated with insulin, mean BMI 37.8, 80 percent female; n=204, 16 weeks
A phase 2 randomised placebo-controlled dose-escalation study measured body weight and waist circumference over 16 weeks, with a placebo-corrected weight reduction of 3.7 percent. The evidence comes from a clinical population with a mean BMI of 37.8, not from people in the healthy range managing their weight. Pramlintide's approval is as a mealtime insulin adjunct in diabetes; the obesity programme did not proceed to registration and no weight-management approval is on file.
Source PubMed 1 primary source read for this row
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PYY3-36
human RCT · direct outcome · 2 graded rows across 2 of 4 conditions
2 graded rows, 1 source
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Excess food intake
human RCT Direct outcome Not approved for this condition
- Who was studied
- 12 obese and 12 lean adults, double-blind placebo-controlled crossover, single intravenous infusion; buffet lunch offered two hours later
Measured calories eaten at a free-choice buffet lunch after a single infusion: down 30 percent in the obese subjects and 31 percent in the lean subjects, with 24-hour calorie intake also reduced in both groups. This is a one-day intake measurement; the study did not follow body weight, so nothing here shows a change in weight.
Source PubMed 1 primary source read for this row
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Obesity
human RCT Surrogate marker Not approved for this condition
- Who was studied
- 12 obese and 12 lean subjects, single intravenous infusion, double-blind placebo-controlled crossover
The study measured caloric intake at a buffet meal and 24-hour food intake after a single infusion; body weight over time was not an endpoint and no trial measuring weight change with PYY3-36 is on file. Food intake stands in for the condition here rather than measuring it.
Source PubMed 1 primary source read for this row
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2 graded rows, 2 sources
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Obesity
human RCT Direct outcome In registered trials
- Who was studied
- adults with BMI >=30, or >=27 with at least one weight-related condition; n=338, 48 weeks
A phase 2 randomised double-blind placebo-controlled trial measured percentage change in body weight at 48 weeks. No phase 3 result and no regulatory approval for any condition is on file.
Source PubMed 1 primary source read for this row
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Fat loss
human RCT Direct outcome In registered trials
- Who was studied
- adults with type 2 diabetes, HbA1c 7.0-10.5%, BMI 25-50; body-composition substudy n=189 randomised, 103 with both baseline and week-36 DXA scans, 36 weeks
A prespecified DXA substudy of a phase 2 randomised placebo-controlled trial measured percent change in total body fat mass at 36 weeks: reductions of 15.2% (4 mg pooled), 26.1% (8 mg pooled) and 23.2% (12 mg) versus 4.5% with placebo. The population was people with type 2 diabetes, not healthy adults seeking body-composition change. The separate phase 2 obesity trial (n=338, 48 weeks, BMI 30+ or 27+ with a weight-related condition) reported scale weight only, so fat loss as distinct from weight loss rests on the diabetes substudy.
Source PubMed 2 primary sources read for this row
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Semaglutide
human RCT · direct outcome · 2 graded rows across 2 of 4 conditions
2 graded rows, 1 source
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Obesity
human RCT Direct outcome Approved for this condition
- Who was studied
- adults with BMI >=30, or >=27 with at least one weight-related coexisting condition, without diabetes; n=1961, 68 weeks
STEP 1, a randomised double-blind placebo-controlled trial, measured percentage change in body weight over 68 weeks alongside lifestyle intervention. The FDA approved semaglutide 2.4 mg for chronic weight management; participants with diabetes were excluded from this trial.
Source PubMed 1 primary source read for this row
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Weight management
human RCT Direct outcome Approved for this condition
- Who was studied
- adults with BMI >=30, or >=27 with at least one weight-related coexisting condition, without diabetes; n=1961, 68 weeks
STEP 1, a randomised double-blind placebo-controlled trial, measured percentage change in body weight over 68 weeks alongside lifestyle intervention, and the FDA approval is specifically for chronic weight management at those BMI thresholds. The evidence comes from a clinical population enrolled by BMI, not from people in the healthy range managing their weight; no trial below those thresholds is on file.
Source PubMed 1 primary source read for this row
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Setmelanotide
human RCT · direct outcome · 2 graded rows across 2 of 4 conditions
2 graded rows, 2 sources
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Obesity
human RCT Direct outcome Approved for this condition
- Who was studied
- patients aged 6 years or older with a clinical diagnosis of Bardet-Biedl or Alstrom syndrome and obesity, n=38 randomised (19 setmelanotide, 19 placebo; 16 Bardet-Biedl and 3 Alstrom in each arm); 14 weeks blinded then 52 weeks open-label, up to 3.0 mg subcutaneously once daily
The primary endpoint was the proportion of patients aged 12 or over with at least a 10% bodyweight reduction after 52 weeks; 32.3% reached it (95% CI 16.7 to 51.4, p=0.0006). The result was recorded as inconclusive in the three-per-arm Alstrom subgroup. Skin hyperpigmentation occurred in 23 of 38 patients and injection site erythema in 18. This trial supported approval as the first drug for obesity in Bardet-Biedl syndrome; the licence covers named genetic and syndromic causes, and no trial on file tests common polygenic obesity. A separate phase 2 open-label trial in 18 patients with acquired hypothalamic obesity reported 16 of 18 reaching a 5% BMI reduction at 16 weeks (PMID 38697184), but that population is not one of the conditions graded here. Rung set from the study's own design wording, "randomised, 14-week double-blind, placebo-controlled".
Source PubMed 1 primary source read for this row
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Excess food intake
human case series Direct outcome Approved for this condition
- Who was studied
- participants aged 6 years or older with severe obesity due to biallelic pro-opiomelanocortin or leptin receptor deficiency, n=10 (POMC trial) and n=11 (LEPR trial), across ten hospitals in seven countries; 12 weeks open-label, an 8-week placebo-controlled withdrawal sequence, then 32 further open-label weeks. The hunger endpoint was assessed in 7 participants per trial aged 12 or over
Hunger was measured directly on the most-hunger item of an 11-point Likert-type scale. Mean change at approximately one year was -27.1% in the POMC trial (n=7, 90% CI -40.6 to -15.0, p=0.0005) and -43.7% in the LEPR trial (n=7, -54.8 to -29.1, p<0.0001). Seven participants per trial is the whole hunger dataset, and there is no placebo comparison for it: the withdrawal sequence was blinded, but the reported hunger figure is the change from baseline on treatment. Injection site reaction was reported in every participant in both trials. Rung set by review: the pivotal POMC and LEPR trials are single-arm and open-label, and the hunger figure is a change from baseline in seven participants per trial with no placebo comparison.
Source PubMed 1 primary source read for this row
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Tirzepatide
human RCT · direct outcome · 2 graded rows across 2 of 4 conditions
2 graded rows, 1 source
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Obesity
human RCT Direct outcome Approved for this condition
- Who was studied
- adults with BMI >=30, or >=27 with at least one weight-related complication, without diabetes; n=2539, 72 weeks
SURMOUNT-1, a phase 3 randomised placebo-controlled trial, measured percentage change in body weight at 72 weeks. The FDA approved tirzepatide for chronic weight management; this trial excluded people with diabetes, who were studied separately in SURMOUNT-2.
Source PubMed 1 primary source read for this row
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Weight management
human RCT Direct outcome Approved for this condition
- Who was studied
- adults with BMI >=30, or >=27 with at least one weight-related complication, without diabetes; n=2539, 72 weeks
SURMOUNT-1, a phase 3 randomised placebo-controlled trial, measured percentage change in body weight at 72 weeks; the FDA approval for chronic weight management carries the same BMI thresholds as enrolment. The evidence comes from a clinical population enrolled by BMI, not from people in the healthy range managing their weight; participants with diabetes were studied separately in SURMOUNT-2.
Source PubMed 1 primary source read for this row
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VK2735
human RCT · direct outcome · 2 graded rows across 2 of 4 conditions
2 graded rows, 1 source
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Obesity
human RCT Direct outcome In registered trials
- Who was studied
- adults with BMI >=30, or >=27 with at least one weight-related comorbidity, BMI <50; n=176, 13 weeks
The VENTURE phase 2 trial of weekly subcutaneous VK2735 set percent change in body weight from baseline to week 13 as its primary outcome. The trial is short and small relative to the registrational obesity programmes, and no approval exists for any condition.
Source ClinicalTrials.gov 1 primary source read for this row
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Weight management
human RCT Direct outcome In registered trials
- Who was studied
- adults with BMI >=30, or >=27 with at least one weight-related comorbidity, BMI <50; n=176, 13 weeks
The VENTURE phase 2 trial of weekly subcutaneous VK2735 set percent change in body weight from baseline to week 13 as its primary outcome. The trial is short and small relative to the registrational obesity programmes, the evidence comes from a population enrolled by BMI rather than from people in the healthy range managing their weight, and no approval exists for any condition.
Source ClinicalTrials.gov 1 primary source read for this row
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Cholecystokinin (CCK)
human RCT · direct outcome · 1 graded row across 1 of 4 conditions
1 graded row, 1 source
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Excess food intake
human RCT Direct outcome Not approved for this condition
- Who was studied
- healthy men, n=15, double-blind placebo-controlled crossover, 20-minute intravenous CCK-8 infusion at 4 ng/kg/min before one ad libitum test meal
Energy intake at a single ad libitum test meal fell during CCK-8 infusion relative to saline, by 56.6 percent in the eight subjects reporting gastrointestinal disturbance and 44.6 percent in the seven without; meal duration and eating rate also fell. The reduction was measured at one meal in healthy volunteers, and the paper's own question was how far nausea and anxiety account for it. An earlier double-blind crossover in eight obese men found six of eight ate less on the same infusion rate.
Source PubMed 2 primary sources read for this row
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1 graded row, 1 source
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Excess food intake
human RCT Direct outcome Not approved for this condition
- Who was studied
- healthy adults, n=9, randomised double-blind crossover, single intravenous infusion at 5.0 pmol/kg/min
Ghrelin increases food intake: every participant ate more from a free-choice buffet during ghrelin infusion than during saline, a mean rise of 28 percent, with higher appetite scores. It was administered to stimulate eating, and this row records an orexigenic effect, the opposite direction to the subject of this page.
Source PubMed 1 primary source read for this row
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1 graded row, 1 source
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Obesity
human RCT Direct outcome Approved for this condition
- Who was studied
- adults with BMI >=30, or >=27 with treated or untreated dyslipidaemia or hypertension, without diabetes; n=3731, 56 weeks
The SCALE Obesity and Prediabetes trial measured change in body weight at 56 weeks against placebo, with diet and exercise in both arms. The FDA approved liraglutide 3.0 mg for weight management; the 1.8 mg product is a separate approval for type 2 diabetes.
Source PubMed 1 primary source read for this row
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1 graded row, 1 source
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Obesity
human RCT Direct outcome In registered trials
- Who was studied
- adults aged 18-75 with BMI >=27 without diabetes; n=387 enrolled, 386 treated, 46 weeks; 233 of 386 completed treatment
A dose-finding phase 2 randomised double-blind placebo-controlled trial with percentage change in body weight at week 46 as the primary endpoint. Roughly 40 percent of treated participants did not complete the treatment period; phase 3 trials are registered and no approval exists.
Source PubMed 1 primary source read for this row
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1 graded row, 1 source
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Fat loss
human RCT Direct outcome Not approved for this condition
- Who was studied
- HIV-infected adults with lipodystrophy and excess abdominal fat; study 1 n=412 (273 drug / 137 placebo), study 2 n=404 (270 / 126); 26-week main phase
Two randomised, double-blind, placebo-controlled trials measured visceral adipose tissue by CT at 26 weeks: mean reductions of 27 cm2 and 21 cm2 versus a 4 cm2 increase and no change on placebo. The FDA approval (EGRIFTA SV) is specifically for reduction of excess abdominal fat in HIV-infected adults with lipodystrophy, a disease population; the label addresses no non-HIV population, and no trial in healthy adults seeking body-composition change is on file.
Source DailyMed — the FDA label 1 primary source read for this row
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Leptin
human case series · direct outcome · 1 graded row across 1 of 4 conditions
1 graded row, 1 source
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Excess food intake
human case series Direct outcome Not approved for this condition
- Who was studied
- women with lipodystrophy and hypoleptinaemia, n=8, open-label recombinant methionyl human leptin for 4 months; no control group
Energy consumed to reach satiation from a standardised food array fell from 2034 to 1135 kcal over four months of leptin injections, with satiation reached sooner and satiety lasting longer. All eight participants were leptin-insufficient, which is the condition being corrected; no measured-intake study on file in people with normal leptin. Metreleptin is approved for the metabolic complications of generalised lipodystrophy and congenital leptin deficiency, not for reducing food intake.
Source PubMed 1 primary source read for this row
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1 graded row, 1 source
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Fat loss
human case series Surrogate marker Not approved for this condition
- Who was studied
- obese insulin-resistant patients with type II diabetes, n=12 recruited, 6 completing 6 weeks; body composition by dual energy x-ray absorptiometry
The only fat-mass measurement on file for IGF-I is incidental to a glucose study: a 2.1% loss in body fat by DXA over six weeks, with no change in total bodyweight. It was not a stated endpoint, there was no control group, and the population was diabetic rather than someone seeking fat loss. No trial has set out to test IGF-I for fat loss, so what exists is one uncontrolled six-week observation in twelve people, half of whom stopped early. Rung set by review: the same twelve uncontrolled patients — one study has one rung.
Source PubMed 1 primary source read for this row
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Brinp-2 Related Peptide (BRP)
animal in vivo · direct outcome · 3 graded rows across 3 of 4 conditions
3 graded rows, 1 source
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5-Amino-1MQ
animal in vivo · direct outcome · 2 graded rows across 2 of 4 conditions
2 graded rows, 1 source
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Obesity
animal in vivo Direct outcome Not approved for this condition
- Who was studied
- diet-induced obese male mice on a high-fat diet, intraperitoneal dosing; no human study on file
Body weight, white adipose tissue mass and adipocyte size were measured in mice given the NNMT inhibitor 5-amino-1MQ. Every figure here is a rodent figure at a rodent dose by injection; no human trial of 5-amino-1MQ for weight has been located.
Source PubMed 1 primary source read for this row
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Fat loss
animal in vivo Surrogate marker Not approved for this condition
- Who was studied
- diet-induced obese mice, systemic administration; no human study located
A potent NNMT inhibitor reduced body weight and white adipose tissue mass in diet-induced obese mice without changing food intake. Adipose mass was measured, not scale weight alone, but the measurement was in mice. No human study of 5-amino-1MQ measuring body weight or body composition is on file.
Source PubMed 1 primary source read for this row
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HGH Frag 176-191
animal in vivo · direct outcome · 2 graded rows across 2 of 4 conditions
2 graded rows, 2 sources
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Obesity
animal in vivo Direct outcome Not approved for this condition
- Who was studied
- obese (ob/ob) and lean C57BL/6J mice, treated for 14 days by mini-osmotic pump; group sizes not stated in the abstract
Bodyweight gain was significantly reduced in obese mice, alongside increased fat oxidation and raised plasma glycerol. Unlike growth hormone, the fragment did not cause hyperglycaemia and did not bind the growth hormone receptor. This is a mouse study and there is no published human counterpart: phase IIa trials in obesity were reported as under way in 2002 (PMID 15134286) and the compound appears in obesity drug-pipeline reviews through 2013, but no trial result for it is indexed in PubMed or Europe PMC. A drug that entered human obesity trials more than twenty years ago and has no published human efficacy data is a stronger fact about the record than any of the animal work. Rung set from the study's own design wording, "mice".
Source PubMed 1 primary source read for this row
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Fat loss
animal in vivo Surrogate marker Not approved for this condition
- Who was studied
- obese Zucker rats given 500 micrograms/kg bodyweight orally each day for 19 days; group sizes not stated in the abstract
Bodyweight gain over 19 days was 15.8 g against 35.6 g in controls, and lipolytic activity in adipose tissue rose. Euglycaemic clamp showed no adverse effect on insulin sensitivity, in contrast to intact growth hormone. What is measured is weight gain prevented and tissue lipolysis, not fat mass on a scan, and the animal is a genetically obese rat. No human measurement of fat loss with this compound exists. Rung set from the study's own design wording, "rats".
Source PubMed 1 primary source read for this row
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Agouti-Related Protein (AgRP)
animal in vivo · direct outcome · 1 graded row across 1 of 4 conditions
1 graded row, 1 source
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1 graded row, 1 source
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Excess food intake
animal in vivo Direct outcome Not approved for this condition
- Who was studied
- rats aged 7-9 weeks, 3 months and 15-18 months, intraperitoneal amylin 0.1-10 mcg/kg, food-deprived before testing
Intraperitoneal amylin reduced food intake dose-dependently in food-deprived rats, mostly within the first two hours, with intake compensated by 24 hours and no effect in non-deprived animals. The human buffet-meal evidence usually attached to amylin was generated with pramlintide, a modified analogue, not with native amylin; no measured-intake study in humans using native amylin is on file.
Source PubMed 1 primary source read for this row
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Nesfatin-1
animal in vivo · direct outcome · 1 graded row across 1 of 4 conditions
1 graded row, 1 source
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Excess food intake
animal in vivo Direct outcome Not approved for this condition
- Who was studied
- rats, intracerebroventricular injection, acute and chronic dosing; no human study on file
Intracerebroventricular nesfatin-1 decreased food intake in rats dose-dependently, and a neutralising antibody increased it; the effect persisted in leptin-receptor-mutant Zucker rats and was blocked by a melanocortin-3/4 antagonist. Delivery was directly into the brain ventricles of rats, and no study has measured food intake in humans given nesfatin-1.
Source PubMed 1 primary source read for this row
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Obestatin
animal in vivo · direct outcome · 1 graded row across 1 of 4 conditions
1 graded row, 1 source
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Excess food intake
animal in vivo Direct outcome Not approved for this condition
- Who was studied
- rats, treated with obestatin isolated from rat stomach; no human study on file
The 2005 isolation paper reported that obestatin suppressed food intake and slowed weight gain in rats. That result has repeatedly failed to replicate: a later rat study found no effect on spontaneous intake in either fed or food-restricted animals and no blocking of ghrelin-stimulated intake, and the proposed GPR39 receptor binding also failed to replicate, leaving the receptor unresolved. No human food-intake study is on file.
Source PubMed 2 primary sources read for this row
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1 graded row, 1 source
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Excess food intake
animal in vivo Direct outcome Not approved for this condition
- Who was studied
- rats, single intracerebroventricular injection of 23.4 nmol and 8-day infusion of 18 nmol/day; no human study on file
Orexin-A increases food intake: a single intracerebroventricular dose increased feeding in satiated rats and prolonged it in fasted rats, and an 8-day infusion raised daytime feeding while lowering night-time feeding, leaving 24-hour intake unchanged. It is administered to stimulate feeding, the opposite direction to the subject of this page, and no measured-intake study in humans is on file.
Source PubMed 1 primary source read for this row
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1 graded row, 1 source
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Fat loss
animal in vivo Surrogate marker Not approved for this condition
- Who was studied
- obese mice and beta-3 adrenergic receptor knock-out mice, 14 days intraperitoneal administration; no readable human study
Chronic intraperitoneal AOD9604 reduced body weight and body fat in obese mice over 14 days; the effect on body weight and lipolysis was absent in beta-3 adrenergic receptor knock-out mice. Human trials of AOD-9604 are described in review articles only: no primary report of any AOD-9604 human trial could be reached, so no human row is graded here and the review accounts are not cited.
Source Oxford Academic 1 primary source read for this row
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1 graded row, 1 source
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Fat loss
animal in vivo Surrogate marker Not approved for this condition
- Who was studied
- mice, including aged and high-fat-diet-fed animals; no human study located
MOTS-c treatment prevented diet-induced obesity and age-dependent and diet-induced insulin resistance in mice, with skeletal muscle identified as the target tissue and AMPK activation as the mechanism. No human study of MOTS-c measuring body weight or body composition is on file.
Source PubMed 1 primary source read for this row
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Checked, and nothing on file
19 compounds were read against these conditions and produced no gradeable row. They are named here rather than left off, because a list of 29 reads identically whether 29 survived 48 or 29 were all anyone thought of.
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Angiotensin I
No rung — nothing on file to grade
Checked against obesity. No study meeting the rubric was found for any of them.
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C-Max on obesity
No rung — nothing on file to grade Not approved for this condition
The search was made by name rather than by condition, because there is no molecule to search for: C-Max has no sequence, no molecular weight, no formula and no registry number on file, and PubChem returns no CID for the name. Nothing to grade against this or any other condition.
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C-Max on fat loss
No rung — nothing on file to grade Not approved for this condition
No study of any kind is matched to this name. Europe PMC hits for the string are the pharmacokinetic parameter Cmax, not a compound.
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C-Max on weight management
No rung — nothing on file to grade Not approved for this condition
No study exists to check. The name is in circulation among vendors and not in the literature.
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C-Type Natriuretic Peptide (CNP) on obesity
No rung — nothing on file to grade Not approved for this condition
Not administered for weight; nothing located.
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Chemerin
No rung — nothing on file to grade
Checked against obesity. No study meeting the rubric was found for any of them.
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CJC-1295 no-DAC on fat loss
No rung — nothing on file to grade Not approved for this condition
No graded evidence exists on this record. Every citation attached to CJC-1295 no-DAC carries a null evidence rung, and the set consists of narrative reviews, an analytical-chemistry identification of the compound in an unknown pharmaceutical preparation, and a netnography of self-reported use. No study measuring body weight or body composition after CJC-1295 no-DAC administration, in humans or animals, is on file. The row is recorded because the compound is widely sold and stacked for this purpose.
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CRH (Corticotropin-Releasing Hormone) on obesity
No rung — nothing on file to grade Not approved for this condition
No administered-CRH weight trial exists in any species with a body weight endpoint that could be graded. CRH appears in obesity research as part of the hypothalamic-pituitary-adrenal axis being measured.
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CRH (Corticotropin-Releasing Hormone) on fat loss
No rung — nothing on file to grade Not approved for this condition
Same as obesity. Nothing administered, nothing measured.
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CRH (Corticotropin-Releasing Hormone) on excess food intake
No rung — nothing on file to grade Not approved for this condition
CRH suppresses feeding in rodents, which is a mechanism observation in an animal, not an administered intervention with a human intake outcome. Nothing retrieved supports a row.
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Endothelin-1 on obesity
No rung — nothing on file to grade Not approved for this condition
Nothing administered. ET-1 appears in this literature as a measured marker of endothelial dysfunction in obese cohorts.
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Enfuvirtide on fat loss
No rung — nothing on file to grade Not approved for this condition
No trial has used enfuvirtide for fat loss. The only fat measurements on file come from the antiretroviral safety substudy above, where fat increased slightly.
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Enfuvirtide on weight management
No rung — nothing on file to grade Not approved for this condition
No trial has used enfuvirtide for weight management; weight appears in the record only as a safety parameter.
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GHRH (Growth Hormone-Releasing Hormone) on obesity
No rung — nothing on file to grade Not approved for this condition
No trial has used this compound against this condition; no weight endpoint was measured in any retrieved study of native GHRH.
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GHRH (Growth Hormone-Releasing Hormone) on fat loss
No rung — nothing on file to grade Not approved for this condition
No trial has used native GHRH against this condition; nothing retrieved measured fat mass after native GHRH.
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GHRH (Growth Hormone-Releasing Hormone) on excess food intake
No rung — nothing on file to grade Not approved for this condition
No study measured food intake after GHRH. The appetite work in the somatotropic axis is ghrelin and its agonists, which act at a different receptor.
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GHRP-1 on obesity
No rung — nothing on file to grade Not approved for this condition
No trial has used this compound against this condition. The appetite work in this peptide family was done with GHRP-2, not GHRP-1.
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GHRP-1 on fat loss
No rung — nothing on file to grade Not approved for this condition
No trial has used this compound against this condition; no study on file measured body fat after GHRP-1.
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GHRP-1 on excess food intake
No rung — nothing on file to grade Not approved for this condition
No study measured food intake after GHRP-1 in any species. The ghrelin-agonist feeding literature uses GHRP-2 and ghrelin itself.
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GHRP-6 on obesity
No rung — nothing on file to grade Not approved for this condition
No trial has used this compound against this condition; no body weight or fat mass endpoint was measured in any retrieved GHRP-6 study.
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GHRP-6 on excess food intake
No rung — nothing on file to grade Not approved for this condition
No study measured food intake after GHRP-6 as an endpoint in its own right. Most GHRP-6 appearances in the appetite literature are as the antagonist D-Lys3-GHRP-6, a blocking tool used to test ghrelin, which is the opposite intervention.
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Hexarelin on obesity
No rung — nothing on file to grade Not approved for this condition
No trial has used this compound against this condition; no weight or fat mass endpoint was measured.
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Hexarelin on fat loss
No rung — nothing on file to grade Not approved for this condition
No trial has used this compound against this condition; nothing retrieved measured body fat.
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Hexarelin on excess food intake
No rung — nothing on file to grade Not approved for this condition
No study measured food intake after hexarelin. The feeding work in this peptide family was done with GHRP-2 and with ghrelin.
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Ipamorelin
No rung — nothing on file to grade
Checked against fat loss. No study meeting the rubric was found for any of them.
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Omentin
No rung — nothing on file to grade
Checked against obesity. No study meeting the rubric was found for any of them.
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Sermorelin
No rung — nothing on file to grade
Checked against obesity. No study meeting the rubric was found for any of them.
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Simonson Alpha 1 on obesity
No rung — nothing on file to grade Not approved for this condition
Searched by name rather than by condition, because there is no molecule to search for. The exact phrase Simonson Alpha 1 returns zero hits in Europe PMC all-time, and no PubMed record matches it; the identity record holds no sequence, formula, registry number or PubChem CID.
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Simonson Alpha 1 on fat loss
No rung — nothing on file to grade Not approved for this condition
No study exists to check. The name does not appear as a phrase anywhere in Europe PMC.
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SS-31
No rung — nothing on file to grade
Checked against fat loss. No study meeting the rubric was found for any of them.
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Vasopressin on obesity
No rung — nothing on file to grade Not approved for this condition
Vasopressin is not administered for weight; copeptin appears in this literature only as an observational marker of risk.
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Vasopressin on fat loss
No rung — nothing on file to grade Not approved for this condition
Same as obesity. No administered-peptide trial with a body composition outcome exists.
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Vaspin
No rung — nothing on file to grade
Checked against obesity. No study meeting the rubric was found for any of them.
What this page does not say
It reports what was measured, in whom, and how directly. It does not say what to take or at what dose, and a position here is a record of study depth rather than a reason to use anything. A compound at the top of this list is the most studied against these conditions; that is not the same claim as the most effective, and nothing on this page makes the second one.
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