| Mechanism | Drug | Disease or Use |
| GLP-1 agonist; potentiation of insulin secretion, inhibition of glucagon secretion | |
| Activation of peroxisome proliferator-activated receptors (PPAR), increase in insulin-stimulated rate of glucose utilization, reduced lipolysis and increased fat storage, reduced c | |
| Short-acting KATP channel blockers, increase insulin secretion | |
| Progesterone receptor agonists | |
| Supplement oxytocin | |
| Estrogen receptor agonists in bone, antagonists in breast, uterus, and brain | |
| Somatostatin receptor agonists, intended to reduce the secretion of growth hormone in response to any stimulus | |
| Growth hormone receptor antagonist, most effective therapy for normalization of IGF-1 | |
| Analogue of amylin (a small peptide normally released from beta cells along with insulin); slows gastric emptying, promotes satiety, inhibits glucagon secretion | |
| 5-α reductase inhibitors, inhibit production of dihydrotestosterone | |
| D2 receptor agonist/weak D1 receptor antagonist, intended to reduce the secretion of growth hormone or prolactin | |
| Cyp 17,20 lyase inhibitor, inhibit production of testosterone | |
| GnRH receptor agonists, intended to block testosterone secretion through downregulation of pituitary GnRH receptors | |
| V1A,V2 receptor antagonist | |
| Androgen receptor antagonist | |
| Inhibition of thyroid hormone synthesis and release, | |
| Androgen receptor agonists | |
| | Mechanism | Drug | Disease or Use |
| Progesterone receptor antagonists | |
| Alternate substrate for thyroperoxidase, inhibition of thyroxin synthesis, inhibition of coupling to form thyroglobulin, inhibition of T4®T3 | |
| Estrogen receptor agonists | |
| Replace or supplement growth hormone | |
| V2 receptor antagonist | |
| Concentration in and destruction of thyroid tissue | |
| Estrogen receptor agonist in bone and uterus, antagonist in breast and brain | |
| Replace or supplement T4 | |
| Replace or supplement T3 | |
| Estrogen receptor partial agonist in brain | |
| Alternate substrate for thyroperoxidase, inhibition of thyroxin synthesis, inhibition of coupling to form thyroglobulin | |
| Decreased hepatic glucose production, potentiation of insulin action in peripheral tissues by increasing cell surface insulin receptors, increasing Glut4 glucose transporters and i | |
| DPP-IV inhibitor; slows breakdown of GLP-1 and GIP | |
| Replace or supplement insulin | |
| V2 receptor agonist, replace or supplement vasopression | |
| Long-acting KATP channel blocker, increases insulin secretion | |
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