30 compounds were read against these 3 conditions; 16 produced a graded row. The other 14 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.

1. 01

   Lixisenatide

   human RCT · direct outcome · 3 graded rows across 3 of 3 conditions

   Type 2 diabetes · Hyperglycaemia · Postprandial hyperglycaemia

   3 graded rows, 2 sources

   1. Type 2 diabetes

      human RCT Direct outcome Approved for this condition

      Who was studied

      patients with type 2 diabetes who had had a myocardial infarction or been hospitalised for unstable angina within the previous 180 days, n=6068, median follow-up 25 months

      ELIXA randomised 6068 patients to lixisenatide or placebo added to local standard of care. The primary endpoint was a cardiovascular composite and showed non-inferiority but not superiority; HbA1c was measured as a secondary outcome. The enrolled population is narrow — recent acute coronary syndrome — and is not the general type 2 diabetes population.

      Source PubMed 1 primary source read for this row

   2. Hyperglycaemia

      human RCT Direct outcome Approved for this condition

      Who was studied

      adults with type 2 diabetes on optimised insulin glargine with or without metformin, n=142, multicentre randomised open-label three-arm, 8 weeks; primary measure was the 4-hour postprandial plasma glucose AUC after a standardised solid breakfast

      Lixisenatide 20 mcg once daily reduced the 4-hour postprandial glucose AUC more than liraglutide 1.2 mg (-108.3 mg/dL.h difference) or 1.8 mg (-83.0 mg/dL.h), with greater slowing of gastric emptying, while HbA1c ended similar across arms (about 6.1-6.2%). Symptomatic hypoglycaemia was more frequent with lixisenatide than with liraglutide in this insulin-treated population — the abstract does not quantify the rates. The measurement is the meal excursion in hours after 8 weeks of dosing, not long-term control.

      Source PubMed 1 primary source read for this row

   3. Postprandial hyperglycaemia

      human RCT Direct outcome Approved for this condition

      Who was studied

      adults with type 2 diabetes on optimised insulin glargine with or without metformin, n=142, multicentre randomised open-label three-arm, 8 weeks; primary measure was the 4-hour postprandial plasma glucose AUC after a standardised solid breakfast

      The primary endpoint was the postprandial excursion itself: lixisenatide 20 mcg once daily reduced the 4-hour post-breakfast glucose AUC more than liraglutide 1.2 mg (-108.3 mg/dL.h difference) or 1.8 mg (-83.0 mg/dL.h), with greater slowing of gastric emptying, while HbA1c ended similar across arms (about 6.1-6.2%). Symptomatic hypoglycaemia was more frequent with lixisenatide than with liraglutide in this insulin-treated population; the abstract does not quantify the rates.

      Source PubMed 1 primary source read for this row

2. 02

   Pramlintide

   human RCT · direct outcome · 3 graded rows across 3 of 3 conditions

   Type 2 diabetes · Hyperglycaemia · Postprandial hyperglycaemia

   3 graded rows, 2 sources

   1. Type 2 diabetes

      human RCT Direct outcome Approved for this condition

      Who was studied

      insulin-treated adults with type 2 diabetes (insulin alone or with sulfonylurea and/or metformin), n=656, 52 weeks; mean age 57 years, diabetes duration 12 years, BMI 34.0 kg/m2, baseline HbA1c 9.1%

      A 52-week double-blind placebo-controlled trial of preprandial pramlintide (60 mcg three times daily, 90 mcg twice daily, or 120 mcg twice daily) added to insulin. HbA1c was the measured glycaemic outcome, falling 0.62 percentage points from baseline at week 52 in the 120 mcg twice-daily arm; weight change was reported alongside it. Approved by the FDA as a mealtime adjunct to insulin, not as monotherapy.

      Source PubMed 1 primary source read for this row

   2. Hyperglycaemia

      human RCT Direct outcome Approved for this condition

      Who was studied

      adults with type 2 diabetes, n=24 in a single-blind randomised crossover (12 on exogenous insulin, 12 managed with diet and/or oral agents); 5-hour intravenous pramlintide or placebo infusion with a test meal one hour in, glucose measured over the following 4 hours

      Postprandial glucose, insulin, C-peptide and lactate were measured over four hours after a test meal. Glucose fell significantly only in the insulin-treated group; in the diet/oral-agent group insulin, C-peptide and lactate fell but mean glucose did not, with individual glucose reductions tracking baseline glycated haemoglobin. This is an acute infusion experiment on the analogue pramlintide, not native amylin; the FDA approval is as a mealtime adjunct to insulin, and the label carries a boxed warning for severe insulin-induced hypoglycaemia.

      Source PubMed 1 primary source read for this row

   3. Postprandial hyperglycaemia

      human RCT Direct outcome Approved for this condition

      Who was studied

      adults with type 2 diabetes, n=24 in a single-blind randomised crossover (12 on exogenous insulin, 12 managed with diet and/or oral agents); 5-hour intravenous pramlintide or placebo infusion with a test meal one hour in, glucose measured over the 4 hours after the meal

      The measurement is exactly the post-meal excursion: plasma glucose, insulin, C-peptide and lactate over four hours after a standardised test meal during a pramlintide or placebo infusion. Postprandial glucose fell significantly only in the insulin-treated group; in the diet/oral-agent group insulin, C-peptide and lactate fell but mean glucose did not. This is an acute infusion experiment on the analogue pramlintide, not native amylin; the FDA approval is as a mealtime adjunct to insulin, and the label carries a boxed warning for severe insulin-induced hypoglycaemia.

      Source PubMed 1 primary source read for this row

3. 03

   Cagrilintide

   human RCT · direct outcome · 2 graded rows across 2 of 3 conditions

   Type 2 diabetes · Hyperglycaemia

   2 graded rows, 1 source

   1. Type 2 diabetes

      human RCT Direct outcome In registered trials

      Who was studied

      adults with type 2 diabetes and BMI 27 kg/m2 or higher on metformin with or without an SGLT2 inhibitor, n=92 (cagrilintide monotherapy arm n=30), 32 weeks; 59 (64%) male, mean age 58 years

      Phase 2 trial (NCT04982575) with change in HbA1c as the primary endpoint; the cagrilintide 2.4 mg monotherapy arm changed HbA1c by -0.9 percentage points at week 32 against -1.8 for semaglutide and -2.2 for the combination. HbA1c was measured directly, alongside bodyweight, fasting plasma glucose and CGM time in range. Cagrilintide is not approved by any regulator for type 2 diabetes.

      Source PubMed 1 primary source read for this row

   2. Hyperglycaemia

      human RCT Direct outcome In registered trials

      Who was studied

      adults with type 2 diabetes and BMI 27 kg/m2 or higher on metformin with or without an SGLT2 inhibitor, n=92 randomised (cagrilintide 2.4 mg monotherapy arm n=30), 32 weeks; 59 (64%) male, mean age 58 years

      No single-dose or meal-test study of cagrilintide is on file: the only glucose data located come from 32 weeks of weekly dosing in a phase 2 trial (NCT04982575) whose primary endpoint was HbA1c, with fasting plasma glucose and continuous glucose monitoring as secondary measures. The abstract reports the fasting glucose and time-in-range figures for the cagrilintide-plus-semaglutide arm rather than for cagrilintide alone; the cagrilintide monotherapy arm changed HbA1c by -0.9 percentage points. No level 2 or 3 hypoglycaemia was reported in the trial. Cagrilintide is not approved by any regulator.

      Source PubMed 1 primary source read for this row

4. 04

   Semaglutide

   human RCT · direct outcome · 2 graded rows across 2 of 3 conditions

   Type 2 diabetes · Hyperglycaemia

   2 graded rows, 2 sources

   1. Type 2 diabetes

      human RCT Direct outcome Approved for this condition

      Who was studied

      adults with type 2 diabetes on a standard-care regimen, n=3297, 104 weeks; 2735 (83.0%) had established cardiovascular disease, chronic kidney disease, or both; the abstract does not state the HbA1c entry threshold

      SUSTAIN-6 randomised 3297 patients to once-weekly semaglutide 0.5 mg or 1.0 mg or placebo for 104 weeks. The primary endpoint was a cardiovascular composite (cardiovascular death, non-fatal myocardial infarction, non-fatal stroke), not glycaemia; HbA1c was measured and reported as a secondary outcome, which is why this is graded direct_outcome. Semaglutide carries FDA approval for glycaemic control in type 2 diabetes.

      Source PubMed 1 primary source read for this row

   2. Hyperglycaemia

      human RCT Direct outcome Approved for this condition

      Who was studied

      adults with type 2 diabetes, n=15 enrolled (13 completed), mean age 58.2 years, 86.7% male, mean HbA1c 6.9%, diabetes duration 3.1 years, BMI 30.8 kg/m2; randomised double-blind placebo-controlled crossover, two 12-week periods, glucose measured across a 5-hour standardised breakfast and an 8-hour fat-rich breakfast

      Oral semaglutide escalated to 14 mg once daily reduced the postprandial glucose area under the curve over five hours by 29% against placebo (treatment ratio 0.71), with a similar reduction after a fat-rich meal and delayed gastric emptying. The measurement here is the meal glucose excursion in hours, not HbA1c over months; the compound was dosed for 12 weeks beforehand, so this is not a single-dose result. Semaglutide is FDA-approved for glycaemic control in type 2 diabetes; the trial did not report hypoglycaemia as an outcome.

      Source PubMed 1 primary source read for this row

5. 05

   Tirzepatide

   human RCT · direct outcome · 2 graded rows across 2 of 3 conditions

   Type 2 diabetes · Hyperglycaemia

   2 graded rows, 2 sources

   1. Type 2 diabetes

      human RCT Direct outcome Approved for this condition

      Who was studied

      adults with type 2 diabetes, n=1879, 40 weeks, open-label; mean baseline HbA1c 8.28%, mean age 56.6 years, mean weight 93.7 kg; background therapy not stated in the abstract

      SURPASS-2 randomised 1879 patients 1:1:1:1 to tirzepatide 5, 10 or 15 mg or semaglutide 1 mg once weekly. The primary endpoint was change in HbA1c from baseline to 40 weeks, so glycaemia was the measured outcome rather than a secondary. This is a head-to-head trial against semaglutide; tirzepatide is FDA-approved for type 2 diabetes.

      Source PubMed 1 primary source read for this row

   2. Hyperglycaemia

      human RCT Surrogate marker Approved for this condition

      Who was studied

      adults with type 2 diabetes on metformin at two German centres, n=117 (tirzepatide 15 mg n=45, semaglutide 1 mg n=44, placebo n=28), 28 weeks of weekly subcutaneous dosing; hyperinsulinaemic-euglycaemic and hyperglycaemic clamps plus mixed-meal testing

      A phase 1 clamp trial measuring insulin secretion and insulin sensitivity rather than glucose itself: clamp disposition index improved against placebo (treatment difference 1.92) and against semaglutide (0.84), with reduced glucose excursions on meal testing. It is graded surrogate_marker because the clamp fixes glucose by design and reports secretion and sensitivity, which stand in for the capacity to control glucose rather than being a glucose result. Nausea occurred in 24% of tirzepatide recipients; tirzepatide is FDA-approved for glycaemic control in type 2 diabetes.

      Source PubMed 1 primary source read for this row

6. 06

   Dulaglutide

   human RCT · direct outcome · 1 graded row across 1 of 3 conditions

   Type 2 diabetes

   1 graded row, 1 source

   1. Type 2 diabetes

      human RCT Direct outcome Approved for this condition

      Who was studied

      men and women aged at least 50 years with type 2 diabetes and either a previous cardiovascular event or cardiovascular risk factors, n=9901, median follow-up 5.4 years; median baseline HbA1c 7.2% (IQR 6.6-8.1), 4589 (46.3%) women

      REWIND randomised 9901 participants to weekly dulaglutide 1.5 mg or placebo across 371 sites. The primary endpoint was a cardiovascular composite; HbA1c was measured at baseline and through follow-up, which is why this is graded direct_outcome rather than surrogate. Dulaglutide is FDA-approved for glycaemic control in type 2 diabetes.

      Source PubMed 1 primary source read for this row

7. 07

   Exenatide

   human RCT · direct outcome · 1 graded row across 1 of 3 conditions

   Type 2 diabetes

   1 graded row, 1 source

   1. Type 2 diabetes

      human RCT Direct outcome Approved for this condition

      Who was studied

      patients with type 2 diabetes with or without previous cardiovascular disease, n=14752 (10782, 73.1%, with previous cardiovascular disease), median follow-up 3.2 years (IQR 2.2-4.4); the abstract does not report the HbA1c entry range

      EXSCEL randomised 14752 patients to extended-release exenatide 2 mg weekly or placebo. The primary endpoint was a cardiovascular composite and was not met for superiority; HbA1c was measured as a secondary outcome, which is the basis for the direct_outcome grade. Exenatide is FDA-approved for glycaemic control in type 2 diabetes.

      Source PubMed 1 primary source read for this row

8. 08

   Liraglutide

   human RCT · direct outcome · 1 graded row across 1 of 3 conditions

   Type 2 diabetes

   1 graded row, 1 source

   1. Type 2 diabetes

      human RCT Direct outcome Approved for this condition

      Who was studied

      patients with type 2 diabetes and high cardiovascular risk, n=9340, median follow-up 3.8 years; the abstract does not report the HbA1c entry range or background therapy

      LEADER randomised 9340 patients to liraglutide or placebo added to standard care. The primary endpoint was a cardiovascular composite; HbA1c was measured as a reported outcome, so the row is direct_outcome, but no glycaemic endpoint was primary here. Liraglutide is FDA-approved for type 2 diabetes.

      Source PubMed 1 primary source read for this row

9. 09

   Retatrutide

   human RCT · direct outcome · 1 graded row across 1 of 3 conditions

   Type 2 diabetes

   1 graded row, 1 source

   1. Type 2 diabetes

      human RCT Direct outcome In registered trials

      Who was studied

      adults aged 18-75 with type 2 diabetes, HbA1c 7.0-10.5% (53.0-91.3 mmol/mol) and BMI 25-50 kg/m2, on diet and exercise alone or stable metformin >=1000 mg daily for at least 3 months, n=281 randomised (275 in the efficacy analysis), 36 weeks

      Phase 2 trial (NCT04867785) with change in HbA1c at 24 weeks as the primary endpoint and HbA1c and bodyweight at 36 weeks as secondary; placebo and 1.5 mg dulaglutide were both comparators. Retatrutide is not approved by any regulator for type 2 diabetes.

      Source PubMed 1 primary source read for this row

10. 10

    Survodutide

    human RCT · direct outcome · 1 graded row across 1 of 3 conditions

    Type 2 diabetes

    1 graded row, 1 source

    1. Type 2 diabetes

       human RCT Direct outcome In registered trials

       Who was studied

       adults aged 18-75 with type 2 diabetes, HbA1c 53-86 mmol/mol (7.0-10.0%) and BMI 25-50 kg/m2, on background metformin, n=413 randomised (411 treated), 16 weeks; mean baseline HbA1c 64.7 mmol/mol (8.07%)

       Phase 2 dose-finding trial (NCT04153929) with absolute change in HbA1c at 16 weeks as the primary endpoint and relative bodyweight change as key secondary; open-label semaglutide up to 1.0 mg was an active comparator. Survodutide is not approved by any regulator for type 2 diabetes.

       Source PubMed 1 primary source read for this row

11. 11

    Exendin-4

    human case series · direct outcome · 2 graded rows across 2 of 3 conditions

    Hyperglycaemia · Type 2 diabetes

    2 graded rows, 1 source

    1. Hyperglycaemia

       human case series Direct outcome Not approved for this condition

       Who was studied

       subjects with type 2 diabetes; study A n=24 dosed twice daily with meals for 5 days, study B n=13 dosed once after an overnight fast with 8 hours of observation; sex, HbA1c range and background therapy not reported in the abstract

       Synthetic exendin-4 (AC2993) lowered postprandial and fasting plasma glucose over hours to days in two early clinical studies. Both had placebo arms but the abstract does not state that allocation was randomised, so the rung is set below human_rct. The measurements are acute — plasma glucose, insulin and glucagon over a single 8-hour observation and across 5 days of mealtime dosing; nothing on file measured a durable glycaemic outcome for the native venom peptide. The marketed synthetic form of this same molecule is exenatide.

       Source PubMed 1 primary source read for this row

    2. Type 2 diabetes

       human case series Surrogate marker Not approved for this condition

       Who was studied

       subjects with type 2 diabetes; study A n=24 dosed twice daily with meals for 5 days, study B n=13 dosed once after an overnight fast with 8 hours of observation; sex, HbA1c range and background therapy not reported in the abstract

       Synthetic exendin-4 (AC2993) reduced postprandial and fasting plasma glucose in two early clinical studies. Both had placebo arms but the abstract does not state that allocation was randomised, so the rung is set conservatively below human_rct. The measured outcomes were plasma glucose, insulin and glucagon concentrations over hours to days; no study on file measured HbA1c for the native venom peptide. The marketed synthetic form of this same molecule is exenatide, which is graded on its own row.

       Source PubMed 1 primary source read for this row

12. 12

    GLP-1 (7-36)

    human case series · direct outcome · 2 graded rows across 2 of 3 conditions

    Hyperglycaemia · Type 2 diabetes

    2 graded rows, 1 source

    1. Hyperglycaemia

       human case series Direct outcome Not approved for this condition

       Who was studied

       patients with type 2 diabetes in poor metabolic control on diet and sulphonylurea, some with added metformin or acarbose, n=10, HbA1c 11.6 +/- 1.7%; single 4-hour intravenous infusion, within-subject placebo comparison

       Native GLP-1 (7-36 amide) infused intravenously at 1.2 pmol/kg/min brought fasting plasma glucose down to normal fasting concentrations within four hours, with insulin and C-peptide rising and glucagon falling. This is an acute physiology experiment on the native hormone over a single session, not a treatment: nothing durable was measured, and the native peptide is not administered as therapy in any regulator-approved form.

       Source PubMed 1 primary source read for this row

    2. Type 2 diabetes

       human case series Surrogate marker Not approved for this condition

       Who was studied

       patients with type 2 diabetes in poor metabolic control on diet and sulphonylurea, some with added metformin or acarbose, n=10, HbA1c 11.6 +/- 1.7%, single 4-hour intravenous infusion

       Intravenous GLP-1 (7-36 amide) at 1.2 pmol/kg/min brought fasting plasma glucose to normal fasting concentrations within 4 hours, with placebo as the within-subject comparison; insulin and C-peptide rose and glucagon fell. This is a single-session physiology study of the native hormone, not a treatment trial: no HbA1c or other durable glycaemic outcome was measured. The therapeutic analogues are graded on their own rows.

       Source PubMed 1 primary source read for this row

13. 13

    IGF-1

    human case series · direct outcome · 1 graded row across 1 of 3 conditions

    Type 2 diabetes

    1 graded row, 1 source

    1. Type 2 diabetes

       human case series Direct outcome Not approved for this condition

       Who was studied

       obese insulin-resistant patients with type II diabetes, n=12 recruited; 9 completed at least 4.5 weeks and 6 completed the full 6 weeks; 100 micrograms/kg subcutaneously twice daily

       Glycated haemoglobin fell from 10.4% before treatment to 8.1% at the end of therapy, fructosamine from 369 to 271 micromol/l, and mean 24-hour glucose from 14.71 to 9.1 mmol/l. Insulin sensitivity on a frequently sampled intravenous glucose tolerance test rose 3.4-fold. There was no control group and no randomisation: every comparison is against the same patients before treatment, so regression, diet change and study attention are not separated from the drug. Half the enrolled patients did not finish the six weeks, and the authors state it remains to be determined whether a dose exists that avoids the side effects while still controlling glucose. IGF-I is not approved for diabetes in any jurisdiction on file; mecasermin's licence is for severe primary IGF-1 deficiency. Rung set by review: twelve patients, every comparison against themselves before treatment; the paper says so in as many words.

       Source PubMed 1 primary source read for this row

14. 14

    Amylin

    human case series · mechanistic only · 2 graded rows across 2 of 3 conditions

    Hyperglycaemia · Postprandial hyperglycaemia

    2 graded rows, 1 source

    1. Hyperglycaemia

       human case series Mechanistic only Not approved for this condition

       Who was studied

       six volunteers, native islet amyloid polypeptide (amylin) infused intravenously at 25 and 50 pmol/kg/min against saline, each session followed by an intravenous glucose bolus of 0.5 g/kg; health status of the volunteers not further characterised in the abstract

       Recorded, and not evidence for this condition

       No study on file has given native amylin to lower a raised blood glucose, and this row is mechanistic only. In the one acute human infusion study located, 25 pmol/kg/min changed neither glucose disposal nor the insulin response to intravenous glucose, and only 50 pmol/kg/min — reaching circulating concentrations above 90 times normal postprandial peaks — reduced the insulin response; the authors concluded that circulating amylin is unlikely to be a hormone influencing carbohydrate metabolism in man at physiological concentrations. Almost all human amylin literature uses the analogue pramlintide rather than the native peptide, which is graded on its own row.

       Source PubMed 1 primary source read for this row

    2. Postprandial hyperglycaemia

       human case series Mechanistic only Not approved for this condition

       Who was studied

       six volunteers, native islet amyloid polypeptide (amylin) infused intravenously at 25 and 50 pmol/kg/min against saline, each session followed by an intravenous glucose bolus of 0.5 g/kg — a bolus, not a meal; health status of the volunteers not further characterised in the abstract

       Recorded, and not evidence for this condition

       No study on file has given native amylin around a meal and measured the post-meal glucose excursion, and this row is mechanistic only. In the one acute human infusion study located, the challenge was an intravenous glucose bolus rather than food: 25 pmol/kg/min changed neither glucose disposal nor the insulin response, and only 50 pmol/kg/min — circulating concentrations above 90 times normal postprandial peaks — reduced the insulin response, leading the authors to conclude circulating amylin is unlikely to influence carbohydrate metabolism in man at physiological concentrations. Almost all human amylin literature uses the analogue pramlintide rather than the native peptide, which is graded on its own row.

       Source PubMed 1 primary source read for this row

15. 15

    GIP (Gastric Inhibitory Peptide)

    human case series · mechanistic only · 2 graded rows across 2 of 3 conditions

    Type 2 diabetes · Hyperglycaemia

    2 graded rows, 1 source

    1. Type 2 diabetes

       human case series Mechanistic only Not approved for this condition

       Who was studied

       patients with mild type 2 diabetes (fasting plasma glucose 7.8 mmol/L, HbA1c 6.3 +/- 0.6%), n=9, compared with 9 age- and weight-matched normal subjects; single hyperglycaemic clamp sessions

       Recorded, and not evidence for this condition

       Synthetic human GIP infused under hyperglycaemic clamp conditions produced an insulin secretory response 54% lower in the type 2 diabetes group than in matched normal subjects, while GLP-1 retained most of its insulinotropic activity. This characterises the physiology of the native hormone and the loss of GIP responsiveness in the disease; it is not administration of GIP as a treatment, and no study on file measured HbA1c or any durable glycaemic outcome with GIP. GIP receptor agonism as a therapy appears only inside the dual and triple agonists graded on their own rows.

       Source PubMed 1 primary source read for this row

    2. Hyperglycaemia

       human case series Mechanistic only Not approved for this condition

       Who was studied

       patients with mild type 2 diabetes (fasting plasma glucose 7.8 mmol/L, HbA1c 6.3 +/- 0.6%), n=9, versus 9 age- and weight-matched normal subjects; single hyperglycaemic clamp sessions

       Recorded, and not evidence for this condition

       No study on file has given GIP to lower a raised blood glucose; this row is mechanistic only. What was measured is the insulin secretory response to synthetic human GIP infused while glucose was held raised by a hyperglycaemic clamp, which was 54% lower in the type 2 diabetes group than in matched normal subjects while GLP-1 kept most of its insulinotropic effect. That characterises the incretin defect in the disease — glucose was clamped by the investigators, not moved by the peptide — and GIP receptor agonism reaches patients only inside the dual and triple agonists graded on their own rows.

       Source PubMed 1 primary source read for this row

16. 16

    MOTS-c

    animal in vivo · mechanistic only · 2 graded rows across 2 of 3 conditions

    Type 2 diabetes · Hyperglycaemia

    2 graded rows, 1 source

    1. Type 2 diabetes

       animal in vivo Mechanistic only Not approved for this condition

       Who was studied

       mice, including high-fat-diet-fed and aged animals; intraperitoneal administration, group sizes and durations as reported in the source; no human participants

       Recorded, and not evidence for this condition

       No study has measured type 2 diabetes in people with MOTS-c: no trial on file has administered it to humans and measured HbA1c, fasting glucose, or any other glycaemic outcome, and this row is mechanistic only. What exists is intraperitoneal administration in mice, where MOTS-c was reported to reduce diet-induced obesity and insulin resistance with glucose infusion rate during clamp as the readout; those figures are murine, and the link to the condition is an argument from rodent physiology rather than a result.

       Source PubMed 1 primary source read for this row

    2. Hyperglycaemia

       animal in vivo Mechanistic only Not approved for this condition

       Who was studied

       mice, including high-fat-diet-fed and aged animals, intraperitoneal administration; group sizes and durations as reported in the source. No human participants have received MOTS-c in any study on file

       Recorded, and not evidence for this condition

       No study has measured blood glucose in people given MOTS-c — no acute infusion, no glucose tolerance test, no meal test, no fasting glucose — and this row is mechanistic only. What exists is intraperitoneal administration in mice, where glucose infusion rate during clamp was the readout and diet-induced insulin resistance was reduced; those figures are murine and by a route not used in humans, so the link to raised blood glucose in a person is an argument from rodent physiology rather than a result.

       Source PubMed 1 primary source read for this row

Checked, and nothing on file

14 compounds were read against these conditions and produced no gradeable row. They are named here rather than left off, because a list of 16 reads identically whether 16 survived 30 or 16 were all anyone thought of.

1. Angiotensin I on type 2 diabetes

   No rung — nothing on file to grade Not approved for this condition

   Nothing located. Angiotensin I appears in this literature as an assay substrate for measuring converting-enzyme activity, not as an intervention.

2. C-Max

   No rung — nothing on file to grade

   Checked against type 2 diabetes. No study meeting the rubric was found for any of them.

3. C-Type Natriuretic Peptide (CNP) on type 2 diabetes

   No rung — nothing on file to grade Not approved for this condition

   Nothing located. CNP appears in this literature as a measured plasma peptide, not an intervention.

4. CRH (Corticotropin-Releasing Hormone) on type 2 diabetes

   No rung — nothing on file to grade Not approved for this condition

   Nothing located. CRH is not administered for glucose control.

5. Endothelin-1 on type 2 diabetes

   No rung — nothing on file to grade Not approved for this condition

   Same. Plasma ET-1 is measured as a marker of vascular damage in diabetes; nobody gives it.

6. GHRH (Growth Hormone-Releasing Hormone) on type 2 diabetes

   No rung — nothing on file to grade Not approved for this condition

   Only mechanistic and safety observations are on file. Glucose tolerance was measured in the somatotropic trials as a safety check rather than as a treatment endpoint, and those trials used an analogue.

7. GHRP-1 on type 2 diabetes

   No rung — nothing on file to grade Not approved for this condition

   No trial has used this compound against this condition; no glycaemic endpoint was measured in any retrieved study.

8. GHRP-2 on type 2 diabetes

   No rung — nothing on file to grade Not approved for this condition

   Only mechanistic and pharmacological work is on file. Glucose and insulin were reported as safety observations in the feeding studies, not as treatment endpoints in a diabetic population.

9. GHRP-6 on type 2 diabetes

   No rung — nothing on file to grade Not approved for this condition

   No trial has used this compound against this condition; no glycaemic endpoint in a diabetic population was measured in any retrieved study.

10. Hexarelin on type 2 diabetes

    No rung — nothing on file to grade Not approved for this condition

    No trial has used this compound against this condition; no glycaemic endpoint in a diabetic population was measured.

11. HGH Frag 176-191 on type 2 diabetes

    No rung — nothing on file to grade Not approved for this condition

    Glucose and insulin appear only as safety comparisons against growth hormone in rodents. No study has dosed a diabetic population of any species with a glycaemic endpoint.

12. HGH Frag 176-191 on hyperglycaemia

    No rung — nothing on file to grade Not approved for this condition

    The rodent record states that the fragment did not induce hyperglycaemia, which is a safety observation about the drug and not a measurement of treating high glucose.

13. Setmelanotide on type 2 diabetes

    No rung — nothing on file to grade Not approved for this condition

    No trial has used setmelanotide against type 2 diabetes. Glycaemic measures appear only as safety laboratory values in the obesity trials, with no diabetic population and no HbA1c endpoint.

14. Setmelanotide on hyperglycaemia

    No rung — nothing on file to grade Not approved for this condition

    No trial has measured glucose as an outcome. The compound is dosed for melanocortin-4 receptor pathway obesity, and glycaemia is not a stated endpoint in any report retrieved.

15. Setmelanotide on postprandial hyperglycaemia

    No rung — nothing on file to grade Not approved for this condition

    No study on file measures a post-meal glucose excursion with setmelanotide, in humans or animals.

16. Simonson Alpha 1

    No rung — nothing on file to grade

    Checked against type 2 diabetes. No study meeting the rubric was found for any of them.

17. Vasopressin on type 2 diabetes

    No rung — nothing on file to grade Not approved for this condition

    Copeptin, the stable fragment of the vasopressin precursor, predicts incident diabetes in cohort studies. That is a measured marker, not an administered intervention, and earns no row.

Browse by goal

• Weight loss — 29 compounds with a graded row, from 48 checked
• Muscle growth — 9 compounds with a graded row, from 20 checked
• Infection & immunity — 23 compounds with a graded row, from 30 checked
• Cardiovascular — 29 compounds with a graded row, from 33 checked
• Healing & recovery — 16 compounds with a graded row, from 29 checked
• Sexual health & fertility — 13 compounds with a graded row, from 28 checked
• Pain — 8 compounds with a graded row, from 19 checked
• Skin & hair — 9 compounds with a graded row, from 33 checked
• Brain & nerve recovery — 7 compounds with a graded row, from 15 checked
• Mood & anxiety — 3 compounds with a graded row, from 12 checked
• Sleep — 9 compounds with a graded row, from 30 checked
• Cognition — 8 compounds with a graded row, from 43 checked
• Inflammation — 5 compounds with a graded row, from 23 checked
• Biological ageing — 8 compounds with a graded row, from 30 checked
• Gut health — 12 compounds with a graded row, from 27 checked