Introduction
Coagulation Factor IX is also known as factor IX, Christmas factor, or F9. It is encoded by the F9 gene located on the X chromosome (Xq27.1-q27.2) in humans. This gene encodes vitamin K-dependent coagulation factor IX that circulates in the blood as an inactive zymogen. This factor is converted to an active form by factor XIa, which excises the activation peptide and thus generates a heavy chain and a light chain held together by one or more disulfide bonds. The role of this activated factor IX in the blood coagulation cascade is to activate factor X to its active form through interactions with Ca+2 ions, membrane phospholipids, and factor VIII. Alterations of this gene, including point mutations, insertions, and deletions, cause factor IX deficiency, which is a recessive X-linked disorder, also called hemophilia B or Christmas disease. Alternative splicing results in multiple transcript variants encoding different isoforms that may undergo similar proteolytic processing. [provided by RefSeq, Sep 2015]

Direction of Drugs Discovery
• F9 Modulator
• F9 Replacement
• F9 Inhibitor
• Developing New Clinical Effects on F9 from Existing Drugs

Drugs
• F9 Modulator- Emicizumab, CSL-654, AMT-060, AAV2-hFIX16, N9-GP
• F9 Replacement- Fidanacogene elaparvovec, SB-FIX
• F9 Inhibitor- Gamma-Carboxy-Glutamic Acid, TTP889, RB-006