Chelsea also intends to initiate a new clinical trial in the fourth quarter of 2013, given guidance regarding the potential need for Chelsea to verify the durability of effect of Northera in a post-marketing study. This study would also include short-term clinical endpoints should the Agency require an additional clinical trial for the approval of Northera.Chelsea recently reported that Study 306B demonstrated statistically significant improvements for Northera compared to placebo in dizziness/lightheadedness at week 1 (p=0.018), the primary endpoint, and increase in standing systolic blood pressure at week 1 (p=0.032), an important secondary endpoint. Treatment with Northera also resulted in a reduction in patient falls and fall-related injuries, also secondary endpoints, although the results were not significant. The safety data were consistent with previous studies, and showed that Northera was well tolerated. Conference Call Today at 9:00 AM ET Chelsea will host a conference call to discuss the guidance today, February 20, at 9:00 AM Eastern Time. Interested investors may participate in the conference call by dialing (877) 638-9567 (domestic) or (720) 545-0009 (international) and referencing conference ID number: 12612161. A replay will be available for one week following the call by dialing (855) 859-2056 for domestic participants or (404) 537-3406 for international participants and referencing conference ID number: 12612161 when prompted. Participants may also access both the live and archived webcast of the conference call on Chelsea's web site at www.chelseatherapeutics.com . About Northera NORTHERA™ (droxidopa), the lead investigational agent in Chelsea Therapeutics' pipeline, is currently in Phase III clinical trials for the treatment of symptomatic neurogenic orthostatic hypotension (NOH) in patients with primary autonomic failure – a group of diseases that includes Parkinson's disease, multiple system atrophy (MSA) and pure autonomic failure (PAF). Droxidopa is a synthetic catecholamine that is directly converted to norepinephrine (NE) via decarboxylation, resulting in increased levels of NE in the nervous system, both centrally and peripherally.