Leiden, The Netherlands, March 26, 2012. Biotech company Pharming Group NV ("Pharming" or "the Company") (NYSE Euronext: PHARM) announced today that it has entered into an agreement with Hyupjin Corporation, a Seoul based Korean specialty pharma company, to commercialise RUCONEST® (recombinant human C1 inhibitor) for the treatment of acute attacks of Hereditary Angioedema (HAE) in the Republic of Korea.

Under the agreement, Hyupjin will drive the regulatory approval in Korea and purchase its commercial supplies of RUCONEST from Pharming at a fixed transfer price.

"The collaboration with a well-established company such as Hyupjin Corporation, as part of our ongoing efforts to extend the commercialisation of RUCONEST is very exciting for us" said Sijmen de Vries, CEO of Pharming. "We are very much looking forward to having RUCONEST distributed by such an experienced partner in Korea. With this agreement with Hyupjin Corporation, we now have two strong partners in Asia for the distribution of RUCONEST, whilst discussions continue with potential partners for other territories."

Mr. Macsan Cho, General Manager of Hyupjin Corporation, said: "In our continuous effort to bring the most innovative therapeutics to patients, this agreement to distribute RUCONEST will now enable us to provide the Korean HAE patients access to this most innovative way to treat their disease. Given our long established relationships in immunology, we feel that RUCONEST complements our existing product portfolio very well and we look forward to getting started."

About RUCONEST (RHUCIN in non-European territories) and Hereditary Angioedema

RUCONEST® (INN conestat alfa) is a recombinant version of the human protein C1 inhibitor (C1INH). RUCONEST is produced through Pharming's proprietary technology in milk of transgenic rabbits and in Europe is approved under the name RUCONESTfor treatment of acute angioedema attacks in patients with HAE. RHUCIN® is an investigational drug in the U.S. and has been granted orphan drug designation for the treatment of acute attacks of HAE, a genetic disorder in which the patient is deficient in or lacks a functional plasma protein C1 inhibitor, resulting in unpredictable and debilitating episodes of intense swelling of the extremities, face, trunk, genitals, abdomen and upper airway. The frequency and severity of HAE attacks vary and are most serious when they involve laryngeal edema, which can close the upper airway and cause death by asphyxiation. According to the U.S. Hereditary Angioedema Association, epidemiological estimates for HAE range from one in 10,000 to one in 50,000 individuals.