Vitamin K (phylloquinone) !

Vitamin K lets the liver activate clotting factors; without it blood takes too long to clot.

Updated 2026-11-01

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Key facts

Coenzyme of γ-glutamyl carboxylase: it adds a carboxyl to glutamate (Gla) residues of factors II, VII, IX and X and of proteins C and S.
Gla residues trap calcium, which anchors the factors to platelet membranes.
Each carboxylation leaves the vitamin as an epoxide; VKORC1 recycles it, and that is warfarin's target.
Newborns have little vitamin K, so it is given at birth to prevent haemorrhagic disease.

Sources: K1 (phylloquinone) in green leaves (spinach, broccoli, cabbage); K2 (menaquinones) is made by colonic bacteria and found in fermented foods.
Reaction: vitamin K hydroquinone, O₂ and CO₂ let γ-glutamyl carboxylase (in the hepatocyte endoplasmic reticulum) turn glutamate into γ-carboxyglutamate.
Recycling: vitamin K epoxide returns to quinone and hydroquinone via vitamin K epoxide reductase (VKORC1); warfarin blocks it.
Other Gla proteins: osteocalcin (bone) and matrix Gla protein (prevents arterial calcification).
Deficiency: newborns without prophylaxis, fat malabsorption, long courses of broad-spectrum antibiotics, malnutrition, liver disease. Mucosal bleeding, bruising, intracranial haemorrhage in infants.
Excess: natural K1 is barely toxic; synthetic menadione can cause haemolysis and jaundice in newborns.
Lab: prothrombin time (PT/INR) lengthens first, because factor VII has the shortest half-life; aPTT lengthens later. PIVKA-II (uncarboxylated prothrombin) confirms deficiency.

A naphthoquinone ring (2-methyl-1,4-naphthoquinone) with a side chain: phytyl in K1, 4 to 13 isoprene units in the K2 forms.
The ring cycles through quinone, hydroquinone (the active form) and epoxide on each turn of the cycle.

Warfarin inhibits VKORC1 and lowers active factors; its effect is reversed with vitamin K and, when urgent, with prothrombin complex concentrate or plasma.
Dietary vitamin K shifts the INR of people on warfarin; a steady intake is advised, not avoidance.
VKORC1 and CYP2C9 variants explain much of the difference in warfarin dose between people.

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Which reaction does the vitamin K-dependent enzyme catalyse?

γ-carboxylation of glutamate residues to calcium-binding γ-carboxyglutamate (Gla) in factors II, VII, IX and X and proteins C and S.

Why does PT/INR lengthen before aPTT in vitamin K deficiency?

Factor VII, in the extrinsic pathway that PT measures, has the shortest half-life (about 6 hours) and falls first.

Where does warfarin act?

It inhibits vitamin K epoxide reductase (VKORC1), blocking vitamin K recycling, so the liver releases uncarboxylated factors.

Why do newborns receive vitamin K at birth?

Little crosses the placenta, breast milk contains little, and the gut has no bacteria yet to make it.

Molecules are shown in their neutral form, as the databases deposit them; in the cell the acids and phosphates are ionised.

Educational information, not medical advice. For any symptom, see a health professional.

Sources: Phylloquinone (CID 5284607) (PubChem, NCBI, 2026) · Public domain; Vitamin K: MedlinePlus Medical Encyclopedia (MedlinePlus, US National Library of Medicine, 2026); Prothrombin Time Test and INR (PT/INR): MedlinePlus Medical Test (MedlinePlus, US National Library of Medicine, 2026); VKORC1 gene: MedlinePlus Genetics (MedlinePlus, US National Library of Medicine, 2026); Textbook of Biochemistry for Medical Students, 6th ed. (Jaypee Brothers Medical Publishers (Vasudevan DM, Sreekumari S, Vaidyanathan K), 2011).

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