Factor XIII 250unit powder and solvent for solution for injection vials
Requires a prescription from a doctor or prescriber
Factor XIII (human) is a heat-treated, lyophilized concentrate of coagulation factor XIII, an endogenous enzyme responsible for the crosslinking of fibrin and an essential component of the coagulation cascade [FDA Label].
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Suspected adverse reactions reported for Factor XIII
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Fibrogammin 250unit powder and solvent for solution for injection vials
Therapeutically similar medicines
Similarity is based on WHO Anatomical Therapeutic Chemical (ATC) classification and on a factual NHS dm+d therapeutic-grouping code prefix. Source data: NHS dm+d via TRUD (OGL v3.0), WHO ATC/DDD Index.
NHS prescribing volume and spending trends
Guidelines from the National Institute for Health and Care Excellence
NICE clinical guidance(3)
Marstacimab for treating severe haemophilia A or B in people 12 years and over without anti-factor antibodies (TA1073)
Efanesoctocog alfa for treating and preventing bleeding episodes in haemophilia A in people 2 years and over (TA1051)
Detecting, managing and monitoring haemostasis: viscoelastometric point‑of‑care testing (ROTEM, TEG and Sonoclot systems) (HTG348)
Source: National Institute for Health and Care Excellence (NICE). Contains public sector information licensed under the Open Government Licence v3.0.
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Codes for healthcare professionals and prescribing systems
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NHS UK identifiers
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SNOMED CT and dm+d codes from NHS TRUD (Technology Reference data Update Distribution), licensed under the Open Government Licence v3.0. BNF code shown is the factual mapping value distributed by NHS Business Services Authority (NHSBSA) in the dm+d supplementary file under OGL v3.0; it is not affiliated with, nor licensed from, the publishers of the British National Formulary. ATC codes from the WHO Collaborating Centre for Drug Statistics Methodology (whocc.no).
Active and completed clinical studies from ClinicalTrials.gov
Source: ClinicalTrials.gov, a database of the U.S. National Library of Medicine (NLM), National Institutes of Health (NIH). Data accessed via ClinicalTrials.gov API v2. Trial information is provided for research purposes and does not constitute medical advice.
Academic studies and reviews for this medicine's active substance
Showing the 50 most relevant studies.
Reviews & meta-analyses: 16 · Randomised trials: 2 · 1968–2026
Showing the 50 most relevant studies, sorted by most relevant.
Song J, Liu L, Ding B, et al.
2026
- Factor XIII Deficiency
- Autoimmune Diseases
- Hemorrhage
L. Sharief, R. Kadir
Haemophilia, 2013
L. Muszbek, Z. Bereczky, Z. Bagoly, et al.
Physiological reviews, 2011
- Cell Physiological Phenomena
- Blood Cells
- Blood Coagulation
Loo Keat Wei, Lyn Griffiths, Cheah Wee Kooi, et al.
Medicina, 2019
Background and aims: Numerous studies examined the association between factors FV, FVII, FXII, and FXIII-A gene polymorphisms and ischemic stroke, but conclusive evidence is yet to be obtained. Thus, this meta-analysis aimed to investigate the novel association of FV rs1800595, FVII rs5742910, FXII rs1801020, and FXIII-A rs5982 and rs3024477 polymorphisms with ischemic stroke risk. Methods: A systematic review was performed on articles retrieved before June 2018. Relevant data were extracted from eligible studies and meta-analyzed using RevMan version 5.3. The strength of association between studied polymorphisms and ischemic stroke risk was calculated as odds ratios and 95% confidence intervals, by applying both fixed- and random-effect models. Results: A total of 25 studies involving 6100 ischemic stroke patients and 9249 healthy controls were incorporated in the final meta-analysis model. Specifically, rs1800595, rs5742910, rs1801020, rs5982, and rs3024477 consisted of 673, 3668, 922, 433, and 404 cases, as well as 995, 4331, 1285, 1321, and 1317 controls, respectively. The pooled analysis indicated that there was no significant association of FV rs1800595, FVII rs5742910, FXII rs1801020, FXIII-A rs5982, and FXIII-A rs3024477 polymorphisms with ischemic stroke risk, under any genetic models (dominant, recessive, over-dominant, and allelic). Conclusions: The present meta-analysis concluded that FV rs1800595, FVII rs5742910, FXII rs1801020, and FXIII-A rs5982 and rs3024477 polymorphisms are not associated with ischemic stroke risk.
Abstract licence: CC BY 4.0
I. Komáromi, Z. Bagoly, L. Muszbek
Journal of Thrombosis and Haemostasis, 2011
- Hemostasis
- Amino Acid Sequence
- Factor XIII
Shiho Amano, Kohei Oka, Yutaka Sato, et al.
Journal of Clinical Medicine, 2022
Factor XIII (FXIII) deficiency is a rare but serious coagulopathy. FXIII is critical in blood coagulation, and FXIII deficiencies can lead to uncontrolled or spontaneous bleeding. FXIII deficiencies can be congenital or acquired; acquired FXIII deficiency can be categorized as autoimmune and non-autoimmune. Immunological tests to measure FXIII inhibitors are required to diagnose acquired FXIII deficiency; however, appropriate test facilities are limited, which increases the turnaround time of these tests. In the case of critical bleeding, delayed test results may worsen prognosis due to delayed treatment. Here, we report a case of acquired FXIII deficiency, followed by a review of FXIII deficiency cases in Japan. We performed a systematic review to investigate the present conditions of the diagnosis and treatment of FXIII deficiency, including the measurement of FXIII inhibitors in Japan. FXIII inhibitor testing was only performed in 29.7 of acquired FXIII deficiency cases. Clinical departments other than internal medicine and pediatrics were often involved in medical treatment at the time of onset. Therefore, it is important for doctors in clinical departments other than internal medicine and pediatrics to consider FXIII deficiency and perform FXIII inhibitor testing when examining patients with prolonged bleeding of unknown cause or persistent bleeding after trauma.
Abstract licence: CC BY 4.0
Akbar Dorgalaleh, Jamal Rashidpanah
Blood Reviews, 2016
- Abortion, Spontaneous
- Blood Coagulation
- Combined Modality Therapy
J. Jung, G. Song, Jaehoon Kim, et al.
Cardiology journal, 2017
K. Karkouti, C. von Heymann, C. Jespersen, et al.
The Journal of thoracic and cardiovascular surgery, 2013
Haslinger C, Hothorn T, Bossung V, et al.
2025
- Postpartum Hemorrhage
- Factor XIII
- Tranexamic Acid
Sources: aggregated from Europe PMC (EMBL-EBI), OpenAlex, Crossref, PubMed and other open scholarly databases. Retracted articles are excluded. Study information is provided for research purposes and does not constitute medical advice.
Pharmacology and chemical data from DrugBank
Key facts
Drug status
Approved
Major interactions
None known
Half-life
2.29 days
Mechanism
Also known as Fibrin Stabilizing Factor (FSF), Factor XIII is an endogenously pr…
Food interactions
None known
Human targets
None mapped
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
1.44 hr
Tmax = 1.72 hr [A32364]
Cmax = 0.9…
Half-life
2.29 days
6.6 days [A32364]
Volume of distribution
51.1 mL
Clearance
0.09 mL
0.25 mL/hr/kg [A32364]
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Also known as Fibrin Stabilizing Factor (FSF), Factor XIII is an endogenously produced coagulation factor and the final enzyme within the blood coagulation cascade. Within the body, FXIII circulates as a heterotetramer composed of 2 A-subunits and 2 B-subunits (A2B2)[A32363]. When activated by thrombin at the site of injury, the FXIII pro-enzyme is cleaved resulting in activation of the catalytic A-subunit and dissociation from its carrier B-subunit. As a result, the active transglutaminase from subunit A cross-links fibrin and other proteins resulting in increased mechanical strength and resistance to fibrinolysis of the fibrin clot. This contributes to enhanced platelet and clot adhesion to injured tissue, thereby improving blood coagulation and maintenance of hemostasis [A18581].
Other drug products with similar structure and function to Factor XIII (human) include DB09310, which is a recombinant form of the A subunit of human coagulation factor XIII. Compared to Factor XIII (human), which is purified from pooled human plasma, DB09310 is produced through recombinant DNA technology where the target protein is grown in yeast and then isolated [FDA Label].
Factor XIII (Human), available as the commercially available product Corifact, is approved by the Food and Drug Administration for routine prophylactic treatment and peri-operative management of surgical bleeding in adult and pediatric patients with congenital FXIII deficiency [FDA Label]. As the half-life of endogenous Factor XIII is long (5-11 days), prophylactic therapy with the replacement of FXIII can be given every 4-6 to maintain hemostasis[A32363].
Known interactions with other medications. Always consult a healthcare professional.
Showing 50 of 92 interactions
A local tolerance study in rabbits demonstrated no clinical or histopathological changes at the injection site after intravenous, intra-arterial or para-venous administration of Corifact.
A thrombogenicity test was performed in rabbits at doses up to 350 units per kg.
Corifact showed no thrombogenic potential at the doses tested.
How the body processes this drug — absorption, distribution, metabolism, and elimination
Tmax = 1.72 hr [A32364]
Cmax = 0.9 ±0.20 units/mL (peak concentration at steady state) [FDA Label]
Cmax = 87.7% (peak concentration at steady state) [A32364]
6.6 days [A32364]
0.25 mL/hr/kg [A32364]
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
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Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Linked compound data from DrugBank Open Data (CC BY-NC 4.0)
Factor XIII (human)
Matched from: Factor XIII
DrugBank citations
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Structured knowledge from the free knowledge base
ATC classifications (Wikidata)
Linked open data from Wikidata (Q423712), a free and open knowledge base operated by the Wikimedia Foundation. Data is available under the Creative Commons CC0 1.0 Public Domain Dedication.