Emicizumab

Emicizumab
Monoclonal antibody
Type Whole antibody
Source Humanized
Target Activated factor IX, factor X
Clinical data
Trade names Hemlibra
Synonyms ACE910
Routes of
administration		 Subcutaneous injection
ATC code
Legal status
Legal status
  • In general: ℞ (Prescription only)
Identifiers
CAS Number
ChemSpider
  • none
UNII
KEGG

Emicizumab (trade name Hemlibra) is a humanized monoclonal antibody for the treatment of haemophilia A, developed by Chugai (a subsidiary of Roche).[1] A Phase I clinical trial found that it was well tolerated by healthy subjects.[2]

In November 2017, it was approved by the US FDA for treatment of haemophilia A patients who had developed resistance to other treatments.[3] It was subsequently approved by the US FDA in April 2018 under the breakthrough therapy designation for treatment of haemophila A patients who have not developed resistance to other treatments.[4]

Mechanism of action

Emicizumab binds to both the activated coagulation factor IX and to factor X, mediating the activation of the latter. This is normally the function of coagulation factor VIII, which is missing in haemophilia A patients.[1][5]

References

  1. 1 2 H. Spreitzer (4 July 2016). "Neue Wirkstoffe - Emicizumab". Österreichische Apothekerzeitung (in German) (14/2016).
  2. ↑ Uchida, N; Sambe, T; Yoneyama, K; Fukazawa, N; Kawanishi, T; Kobayashi, S; Shima, M (2016). "A first-in-human phase 1 study of ACE910, a novel factor VIII–mimetic bispecific antibody, in healthy subjects". Blood. 127 (13): 1633–1641. doi:10.1182/blood-2015-06-650226. PMC 4817308. PMID 26626991.
  3. ↑ "Roche hemophilia drug wins FDA nod, with a warning". Reuters. 2017-11-17.
  4. ↑ "FDA Grants Roche Breakthrough Therapy Designation on Hemophilia Drug". BioPharm International. UBM. 19 April 2018. Retrieved 2018-04-20.
  5. ↑ Shima, M; Hanabusa, H; Taki, M; Matsushita, T; Sato, T; Fukutake, K; Fukazawa, N; Yoneyama, K; Yoshida, H; Nogami, K (2016). "Factor VIII-Mimetic Function of Humanized Bispecific Antibody in Hemophilia A". New England Journal of Medicine. 374 (21): 2044–53. doi:10.1056/NEJMoa1511769. PMID 27223146.


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