Positive Interim Data From Phase 2 Study of NPSP558 (Parathyroid Hormone 1-84) for Hypoparathyroidism Reported at ASBMR Annual Meeting

September 15, 2008

At the 30th Annual Meeting of the American Society for Bone and Mineral Research (ASBMR), positive interim data were presented from an investigator-initiated Phase 2 proof-of-concept study of NPSP558, the proprietary recombinant full-length human parathyroid hormone (PTH 1-84) under development by NPS Pharmaceuticals, Inc. (NASDAQ: NPSP) for the treatment of hypoparathyroidism. In one plenary poster and two oral presentations, the interim data demonstrated that treatment with PTH 1-84 had a beneficial effect on abnormal bone skeletal properties in patients with hypoparathyroidism, a rare condition typified by insufficient or complete absence of parathyroid hormone and characterized by atypical structural and dynamic properties of bone. There is currently no approved therapy for hypoparathyroidism.

The open-label Phase 2 study of PTH 1-84 for patients with chronic hypoparathyroidism is evaluating the effects of every-other-day subcutaneous injections of 100 ug of the drug on bone structure and turnover. This study is ongoing at Columbia University with John P. Bilezikian, MD, serving as the principal investigator. The three studies being reported by the team are supported separately by the U.S. Food and Drug Administration’s (FDA) Office of Orphan Products Development Grant Program and the National Institutes of Health. NPS is currently preparing to initiate a pivotal registration study to demonstrate the safety and efficacy of NPSP558 for hypoparathyroidism, which it expects to begin in 2008.

The three ASBMR presentations are summarized below.

Plenary Poster Session

Presentation F485: “PTH Increases Bone Turnover in Hypoparathyroidism” by Rubin et al.

Mishaela R. Rubin, MD, Dr. Bilezikian and colleagues measured biochemical markers of bone turnover in 12 patients with chronic hypoparathyroidism at baseline and at monthly intervals during two years of treatment with PTH 1-84. With treatment, markers of bone formation and resorption increased significantly, peaked at five to nine months and returned to baseline levels by two years. The changes in bone turnover markers predicted measurements of turnover in bone biopsies collected after one or two years of treatment. The authors concluded that bone turnover is low in patients with chronic parathyroid hormone deficiency and that the administration of PTH 1-84 increases bone turnover. They also noted that additional data are needed to determine whether these changes lead to long-term effects on skeletal dynamics and on bone strength.

Oral Session

Presentation 1036: “PTH Reverses Abnormal Bone Remodeling and Structure in Hypoparathyroidism” by Rubin et al.

Bone biopsies were performed before (n=16) and after one (n=9) or two (n=7) years of treatment with PTH 1-84 in patients with chronic hypoparathyroidism. Treatment with PTH 1-84 restored atypical structural and dynamic skeletal properties towards normal. The dynamic changes occurred within the first year of therapy and most histomorphometric measures of bone remodeling returned towards baseline levels after two years of treatment when further structural changes became apparent. Drs. Rubin and Bilezikian concluded that, while additional data are needed to determine whether these changes have an impact on bone strength, PTH 1-84 appears to be a highly beneficial therapy for hypoparathyroidism.

Oral Session

Presentation 1146: “Circulating Osteoblast Lineage Cells Increase with PTH Treatment of Hypoparathyroidism” by Rubin et al.

To evaluate the hypothesis that treatment with PTH 1-84 increases bone formation, at least in part by influencing the supply and distribution of cells of osteoblast lineage. Dr. Rubin and colleagues compared the percentage of circulating osteoblast lineage cells from nine subjects with hypoparathyroidism at baseline to an age-, sex-, and menopausal status-matched control group. At baseline, the percentage of circulating osteoblast lineage cells was more than 50% lower in the hypoparathyroidism group versus the control group. With PTH 1-84 treatment, the hypoparathyroidism patients experienced a clinically and statistically significant increase in the number of circulating osteoblast lineage cells to levels that, at the peak, were more than 4-fold greater than baseline. The authors concluded that the close association with biochemical and histomorphometric indices of bone formation suggests that these circulating cells with osteoblast characteristics might be representative of osteoblast activities in bone.

Recent Publications on Hypoparathyroidism

Three recent peer-reviewed publications provide new insights into the complications associated with hypoparathyroidism and its current treatment. “Hypoparathyroidism,” by Dr. Shoback appeared in the July 24, 2008 issue of the New England Journal of Medicine (N Engl J Med 2008; 359:391-403). “Dynamic and Structural Properties of the Skeleton in Hypoparathyroidism,” by Drs. Rubin and Bilezikian was published online on August 6, 2008 in the Journal of Bone and Mineral Research (0.1359/jbmr.080803). “Hypoparathyroidism: Is it time for replacement therapy?” by Drs. Horwitz and Stewart was published in the September 2008 issue of the Journal of Clinical Endocrinology and Metabolism.

About Hypoparathyroidism

NPS has estimated that approximately 65,000 patients suffer from hypoparathyroidism in the U.S. It is one of the few remaining hormone deficiency states without an approved replacement therapy. Because the primary role of parathyroid hormone is to maintain normal calcium levels in blood, the major consequence of its absence is low circulating calcium levels (hypocalcemia). Symptoms of hypocalcemia range from tingling of the hands, fingers, and mouth, to serious muscle cramping in severe cases or, in extreme situations, to tetany or convulsions. The goal of currently available treatments for hypoparathyroidism, which include life-long oral supplementation with calcium and active vitamin D metabolites or analogs, is to prevent symptoms. Severe hypocalcemia can be life threatening and is often treated with intravenous calcium. However, therapies designed to restore normal calcium levels can be accompanied by excessive urinary calcium excretion (hypercalciuria) which can lead to deposition of calcium in the kidney, stone formation and renal insufficiency. Calcification can also occur in other soft tissues including brain and ocular lens, leading to structural damage and a loss of function, as seen in premature cataracts, and even Parkinsonism. Since PTH is the major regulator of bone remodeling, bone turnover is low in hypoparathyroidism. This low turnover state leads to increased mineralization of the skeleton and increased bone mineral density. However, despite the high bone density, increased skeletal fragility has been described. F. J. A. de Paula and colleagues, Internal Medicine, School of Medicine of Ribeirao Preto, University of Sao Paulo, Ribeirao Preto, Brazil, reported at the 2008 Annual Meeting of the American Society for Bone and Mineral Research that over 50% of their patients with hypoparathyroidism had at least one vertebral deformity.

Because it mimics the action of natural parathyroid hormone, NPSP558 has the potential to treat this chronic condition and return the body to a physiological or “eucalcemic” state. In 2007, the U.S. Food and Drug Administration granted NPS Pharmaceuticals orphan drug status for NPSP558 for the treatment of hypoparathyroidism.

About NPSP558 (parathyroid hormone 1-84 (rDNA origin) injection)

NPSP558 is a recombinant full-length human parathyroid hormone (PTH 1-84). NPS is finalizing its protocol for a pivotal registration study to demonstrate the safety and efficacy of NPSP558 for hypoparathyroidism. NPS’s partner Nycomed markets PTH 1-84 in the European Union as Preotact(R) for the treatment of osteoporosis in post-menopausal women at high risk of fractures. In 2007, the FDA granted orphan drug status for NPSP558 for the treatment of hypoparathyroidism.

About NPS Pharmaceuticals

NPS Pharmaceuticals is developing specialty therapeutics for gastrointestinal and endocrine disorders with high-unmet medical needs. The company is currently advancing two late-stage programs. Teduglutide, a proprietary analog of glucagon-like peptide-2, is in Phase 3 clinical development for intestinal failure associated with short bowel syndrome as GATTEX(TM) and in preclinical development for gastrointestinal mucositis and necrotizing enterocolitis. NPSP558 (parathyroid hormone 1-84 (rDNA origin) injection) is in Phase 2 clinical development as a hormone therapy for hypoparathyroidism. NPS complements its proprietary programs with a royalty-based portfolio of products and product candidates that includes strategic partnerships with Amgen, GlaxoSmithKline, Kirin, and Nycomed. Additional information is available at http://www.npsp.com.

“NPS” and “NPS Pharmaceuticals” are the company’s registered trademarks. Preotact(R) is the company’s registered trademark in the U.S. All other trademarks, trade names or service marks appearing in this press release are the property of their respective owners.

Statements made in this press release, which are not historical in nature, constitute forward-looking statements for purposes of the safe harbor provided by the Private Securities Litigation Reform Act of 1995. These statements are based on the company’s current expectations and beliefs and are subject to a number of factors and uncertainties that could cause actual results to differ materially from those described in the forward-looking statements. Risks associated to NPS’s business include, but are not limited to, the risk of not successfully executing its preclinical and clinical studies and not gaining marketing approvals for GATTEX and NPSP558, the risks associated with the implementation of a new business strategy, the risks associated with the company’s auction-rate securities, as well as other factors expressed in NPS’s periodic filings with the U.S. Securities and Exchange Commission, including its Annual Report on Form 10-K/A and Form 10-Qs. All information in this press release is as of the date of this release and NPS undertakes no duty to update this information.

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