Heparin, enoxaparin, warfarin, DOACs, protamine, andexanet, idarucizumab, TXA, DDAVP
Indirect thrombin inhibitor
Activates antithrombin → inactivates IIa (thrombin) and Xa.
Antifibrinolytic (lysine analog)
Reversibly binds plasminogen, blocking conversion to plasmin → preserves fibrin clot.
Heparin antagonist
Strongly basic (positive-charge) protein binds to highly acidic (negative-charge) heparin → inactive ionic complex → renal excretion. 1 mg protamine neutralizes ~100 units heparin.
Synthetic vasopressin V2-receptor agonist
Selective V2 agonist (renal water retention + Factor VIII/vWF release from endothelial Weibel-Palade bodies). NO V1 vasopressor activity at therapeutic dose.
Vitamin K antagonist oral anticoagulant
Inhibits vitamin K epoxide reductase (VKORC1) → depletes reduced vitamin K → ↓ synthesis of factors II, VII, IX, X and proteins C/S. Full effect takes days (waits for existing factor decay).
Low-molecular-weight heparin (LMWH)
Antithrombin-mediated inhibition, weighted toward factor Xa over IIa (~3.8:1). More predictable than UFH — no routine monitoring.
Low-molecular-weight heparin (LMWH)
Antithrombin-mediated factor Xa > IIa inhibition. Similar profile to enoxaparin; preferred LMWH in cancer-associated VTE (CLOT trial).
Low-molecular-weight heparin (LMWH)
Antithrombin-mediated factor Xa > IIa inhibition; higher mean molecular weight than enoxaparin (anti-Xa:IIa ~1.9:1).
Synthetic indirect factor Xa inhibitor (pentasaccharide)
Binds antithrombin → selective, exclusive factor Xa inhibition (no IIa activity). Does NOT cause HIT — safe alternative in HIT patients.
Direct oral anticoagulant — factor Xa inhibitor
Directly binds and inhibits free + clot-bound factor Xa. Predictable, fixed dosing, no routine monitoring.
Direct oral anticoagulant — factor Xa inhibitor
Direct factor Xa inhibitor. Lowest bleeding risk among DOACs in many comparisons; least renal dependence (~27% renal).
Direct oral anticoagulant — direct thrombin (IIa) inhibitor
Directly and reversibly inhibits thrombin (factor IIa), both free and clot-bound. Prodrug (dabigatran etexilate).
Parenteral direct thrombin inhibitor (DTI)
Directly and reversibly inhibits thrombin. HEPATICALLY cleared — the DTI of choice in HIT with renal failure.
Parenteral direct thrombin inhibitor (DTI)
Directly, reversibly inhibits thrombin. Short half-life; predictable. Used in PCI and as a heparin alternative in HIT.
Monoclonal antibody fragment — dabigatran reversal agent
Humanized Fab that binds dabigatran with ~350× the affinity of thrombin → immediate, complete neutralization.
Recombinant modified factor Xa decoy — Xa-inhibitor reversal agent
Catalytically inactive factor Xa 'decoy' that binds and sequesters rivaroxaban/apixaban (and, off-label, edoxaban/LMWH/fondaparinux), restoring endogenous Xa activity.
Prothrombin complex concentrate (factors II, VII, IX, X + proteins C/S)
Replaces the vitamin-K-dependent factors → rapid restoration of coagulation. Small volume, fast, no cross-match.
Activated prothrombin complex concentrate (aPCC)
Contains activated factor VII plus factors II, IX, X → 'bypasses' factor VIII/IX. Used for hemophilia with inhibitors and some DOAC-associated bleeding.
Fat-soluble vitamin — warfarin reversal / factor synthesis cofactor
Cofactor for γ-carboxylation of factors II, VII, IX, X and proteins C/S. Restores warfarin-inhibited synthesis over hours.
Antifibrinolytic (lysine analogue)
Binds plasminogen lysine-binding sites → blocks plasmin formation → stabilizes clot. Same mechanism as TXA (~10× less potent).
Recombinant activated factor VII (procoagulant)
Activates the extrinsic pathway at the site of tissue-factor exposure → thrombin burst. Localized hemostasis.
Antihemophilic factor (recombinant or plasma-derived)
Replaces deficient factor VIII → restores intrinsic-pathway clotting. Dosing based on the rule that 1 unit/kg raises factor VIII activity ~2%.