rs699 — AGT Met235Thr
Risk factor · ~42% global (Thr allele)
rs699 in angiotensinogen (AGT) increases plasma AGT levels by 10-20%, contributing to hypertension risk. It is one of the most replicated hypertension-associated variants and influences response to antihypertensive medications.
Molecular Mechanism
The Met235Thr substitution is in linkage disequilibrium with a promoter variant that increases AGT transcription. Higher circulating angiotensinogen provides more substrate for renin, increasing angiotensin II production and blood pressure.
Peptide Therapeutic Relevance
Renin inhibitor peptides and angiotensinogen-targeting peptides are therapeutic candidates. PepFold designs peptides that could specifically modulate the angiotensin pathway based on individual AGT genotype.
Condition: Hypertension (Essential)
Essential hypertension affects 1.3 billion adults worldwide. AGT (rs699) and AGTR1 (rs5186) variants modulate the renin-angiotensin-aldosterone system (RAAS), the primary pharmacological target for blood pressure control.
Prevalence: 1.3 billion adults worldwide (~30% of adult population)
Related Variants
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