Peptide Library

Binds thrombin directly at two sites and blocks it from making fibrin; thrombin then slowly cleaves the peptide, so the block is short-lived and reversible

Reversibly occupies the platelet glycoprotein IIb/IIIa receptor so fibrinogen cannot cross-link platelets — the final common step of platelet clumping

Activates natriuretic peptide receptor-A, raising cGMP, which widens arteries and veins, lowers filling pressures, and promotes salt and water loss through the kidney

Binds calcitonin-receptor-like receptor paired with RAMP2 or RAMP3, raises cAMP, widens blood vessels and — importantly — stabilises the barrier between blood and tissue

Activates the APJ receptor to increase heart contractility without raising oxygen cost much, widen blood vessels via nitric oxide, and oppose the angiotensin II arm of the renin–angiotensin system

Acts chiefly at the Mas receptor to oppose angiotensin II: widening vessels, reducing fibrosis and inflammation, and limiting cell proliferation

Activates the RXFP1 receptor to widen blood vessels, increase blood flow to the kidney, and suppress fibrosis — a hormone that remodels connective tissue

Urocortin 1 activates both CRF receptors (CRF-R1 and R2); urocortins 2 and 3 act selectively at CRF-R2, which in the heart and vessels means vasodilation and increased contractility rather than a stress response

Released when the heart is stretched by too much blood volume or pressure; act on the kidney to excrete sodium and water, relax blood vessels, and switch off the renin–angiotensin–aldosterone and sympathetic systems — the heart's own…

The most powerful vasoconstrictor the body makes: a local signal that tightens blood vessels, thickens their walls over time and drives fibrosis — overactive in pulmonary hypertension, resistant hypertension and some kidney diseases

A local inflammatory mediator: dilates blood vessels, makes capillaries leak fluid (swelling), triggers pain nerves and causes cough and airway constriction — useful in tissue defence, harmful when overproduced as in hereditary angioedema

Bivalent, essentially irreversible direct thrombin inhibitor — one end occupies thrombin's active site, the other its fibrinogen-binding exosite — blocking clot formation without needing antithrombin and without being neutralised by…

Slowly cleaved in the body to lysine-vasopressin, which constricts splanchnic (gut) arteries via V1 receptors, lowering portal pressure and redirecting blood to the kidneys

Activates AT1 receptors on blood-vessel muscle to constrict arteries and raise blood pressure; also prompts aldosterone and vasopressin release and sympathetic activation

Mimics hepcidin, the liver hormone that controls iron: it triggers degradation of ferroportin, trapping iron in gut cells and macrophages, which lowers the iron available to the bone marrow and so restrains red-cell overproduction

Binds PCSK9 in the circulation and blocks it from degrading LDL receptors, so the liver clears more LDL cholesterol from the blood