Halofuginone
| Systematic (IUPAC) name | |
|---|---|
| 7-Bromo-6-chloro-3-[3-[(2S,3R)-3-hydroxy-2-piperidinyl]-2-oxopropyl]-4-quinazolinone | |
| Clinical data | |
| AHFS/Drugs.com | International Drug Names |
| Pregnancy cat. | ? |
| Legal status | ? |
| Identifiers | |
| CAS number | 55837-20-2 |
| ATCvet code | QP51AX08 |
| PubChem | CID 400772 |
| ChemSpider | 355164 |
| UNII | L31MM1385E |
| ChEMBL | CHEMBL1199540 |
| Chemical data | |
| Formula | C16H17BrClN3O3 |
| Mol. mass | 414.68 g/mol |
| SMILES | eMolecules & PubChem |
|
|
| |
|
Halofuginone is a coccidiostat used in veterinary medicine. It is a synthetic halogenated derivative of febrifugine, a natural quinazolinone alkaloid which can be found in the Chinese herb Dichroa febrifuga (Chang Shan).[1] Collgard Biopharmaceuticals is developing halofuginone for the treatment of scleroderma and it has received orphan drug designation from the U.S. Food and Drug Administration.[2]
Halofuginone inhibits the development of T helper 17 cells, immune cells that play an important role in autoimmune disease, but it does not affect other kinds of T cells which involved in normal immune function.[3] Halofuginone therefore has potential for the treatment of autoimmune disorders.[4]
Halofuginone is also an inhibitor of collagen type I gene expression and as a consequence it may inhibit tumor cell growth.[1]
[edit] References
- ^ a b Halofuginone hydrobromide, NCI Drug Dictionary
- ^ Halofuginone Receives FDA Orphan Drug Status For Scleroderma, March 10, 2000
- ^ Sundrud, M. S.; Koralov, S. B.; Feuerer, M.; Calado, D. P.; Kozhaya, A. E.; Rhule-Smith, A.; Lefebvre, R. E.; Unutmaz, D. et al (2009). "Halofuginone Inhibits TH17 Cell Differentiation by Activating the Amino Acid Starvation Response". Science 324 (5932): 1334–8. doi:10.1126/science.1172638. PMC 2803727. PMID 19498172. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2803727.
- ^ A new lead for autoimmune disease: A small-molecule drug inhibits Th17 cells, eases symptoms in mouse model, June 4, 2009