Class Explorer · Endocrine
Diabetes agents
A mechanistically diverse family: less hepatic glucose (metformin), urinary glucose disposal (SGLT2i), incretin amplification (GLP-1 RA, DPP-4i), insulin release (sulfonylureas), insulin itself.
Members
MetforminFirst among diabetes drugs: effective, weight-neutral, and it does not cause hypoglycemia by itself.EmpagliflozinThe SGLT2 inhibitor that turned a diabetes drug into heart-failure and kidney therapy.DapagliflozinA glucose drug that turned out to be a heart and kidney drug.
Also in this class: Semaglutide (GLP-1 RA, weight and CV benefit) · Gliclazide (sulfonylurea, hypoglycemia) · Sitagliptin (DPP-4i, neutral) · Insulins (the ceiling therapy). Full pages arrive as the library grows.
Compare the members
Metformin
- HbA1c effect
- ~1-1.5%
- Hypoglycemia alone
- No
- Beyond glucose
- Weight-neutral, first line
Empagliflozin
- HbA1c effect
- ~0.5-0.8%
- Hypoglycemia alone
- No
- Beyond glucose
- HF + CKD protection
Shared across the class
- Indications
- Type 2 diabetes, individualized by comorbidity
- Adverse effects
- Hypoglycemia only with insulin and secretagogues, the family's most important internal split
- Contraindications
- Agent-specific; renal function gates several
- Monitoring
- HbA1c every 3-6 months · eGFR (metformin gate, SGLT2 dip) · Weight · Hypoglycemia history with secretagogues/insulin
What makes each agent different
- Organ-protection era: SGLT2 inhibitors and GLP-1 RAs are chosen for hearts, kidneys, and weight, not just HbA1c.
- Hypoglycemia mapping: sulfonylureas and insulin cause it; metformin, SGLT2i, GLP-1 RA, DPP-4i essentially do not alone.
- Sick-day rules: metformin and SGLT2 inhibitors pause in dehydration; insulin never simply stops.
The question is no longer 'what lowers sugar' but 'which comorbidity chooses the second agent'.
Last reviewed 2026-08-15 · Goodman & Gilman's The Pharmacological Basis of Therapeutics, 14th ed.