近日，FDA已同意快速审批GSK和美国人类基因组科学公司（HGS）合作推出的系统性红斑狼疮新药—Benlysta(belimumab)，得到了FDA同意快速审批，此审批工作有望于今年12月9日完成。

Benlysta是一种蛋白质疗法药，主要用于医治系统性红斑狼疮（SLE）。

Benlysta是一种BLyS抑制剂类新型药物，也是在同类药当中首个完成Ⅲ期临床实验的产品。早在今年6月4日，GSK也向欧洲药监局递交了该药的销售申请。

Benlysta申请内容包括药物的两项关键Ⅲ期临床实验数据，参加这两次实验的受试者达1684人，均为SLE患者。实验结果显示，这种静脉注射制剂与目前的标准药联用之后，能够抑制病情的发展，并且还能防止疾病的突然发作。

如果Benlysta最后能获准在美国上市，则能为缺乏特异性治疗药物的SLE患者提供一种有效的选择，是SLE患者的福音。50多年来，还没有任何的SLE新药通过批准。

在综合指标对疗效的评价上，belimumab治疗组显效率为46%，安慰剂组为29% (P = 0.006)。在第76周时，治疗组显效率为56%。belimumab治疗有效的患者的活化B细胞减少了36%，无效患者减少了20% (P<0.05)。抗双链DNA抗体治疗组降低53%，无效患者则为38% (P<0.05)。而且belimumab治疗有效的患者在第52周时的SF－36健康量表平均为增加4.1，治疗无效者仅增加1.0(P < 0.001)。

希腊Crete大学Boumpas教授主持的委员会刚刚制定了欧洲SLE治疗指南。他评价说，这是一项规模很大的研究，该研究小组首次采用了红斑狼疮患者的综合效应评价指标，成功地证实了以前关于抑制B细胞能够改善红斑狼疮患者症状的观察结果。但其疗效中等，所以应与其他方法结合以获得更好的治疗结果

红斑狼疮是一种多发于青年女性的累及多脏器的自身免疫性的炎症性结缔组织病。近年来中西结合的治疗，皮质类固醇和免疫抑制剂的合理应用，使本病的预后有较大的改善，但还是缺乏特异性治疗药物。Benlysta研发成功，有望为全球红斑狼疮患者带来更多的获益。

HUMAN GENOME SCIENCES ANNOUNCES PRESENTATION OF ADDITIONAL PHASE 3 SLE STUDY RESULTS FOR BENLYSTA® (BELIMUMAB) AT INTERNATIONAL CONGRESS ON SLE

ROCKVILLE, Maryland – June 25, 2010 – Human Genome Sciences, Inc. (Nasdaq: HGSI) today announced the presentation of additional results from BLISS-76, one of two pivotal Phase 3 trials of BENLYSTA® (belimumab) in seropositive patients with systemic lupus erythematosus (SLE). The additional data will be presented in Vancouver at the 9th International Congress on Systemic Lupus Erythematosus on Friday and Saturday, June 25-26.

“The BLISS-76 Phase 3 results presented at the International Congress on SLE include new data showing that belimumab treatment, consistent with its mechanism of action, resulted in selective and significantly greater reductions in levels of B-cell and plasma B-cell subsets, with significant preservation of memory B-cells,” said William W. Freimuth, M.D., Ph.D., Vice President, Clinical Research – Immunology, Rheumatology and Infectious Diseases, HGS. “Importantly, belimumab did not significantly affect the ability of SLE patients to maintain a protective response to vaccines, a finding that is consistent with the preservation of memory B-cells.”

KEY BLISS-76 FINDINGS PRESENTED AT THE INTERNATIONAL CONGRESS ON SLE

BLISS-76 Patient Response Rates (SRI)

BLISS-76 data recently presented at the 2010 Congress of the European League Against Rheumatism (EULAR) demonstrated that belimumab 10 mg/kg plus standard of care met the primary endpoint of the Phase 3 study by achieving a statistically significant improvement in patient response rate as measured by the SLE Responder Index (SRI) at Week 52, compared with placebo plus standard of care. At Week 76, belimumab plus standard of care also showed higher response rates compared with placebo plus standard of care as measured by SRI; however, this major secondary endpoint did not reach statistical significance.

• The SRI defines patient response by an improvement in SELENA SLEDAI score of 4 points or greater, with no clinically significant BILAG worsening, and no clinically significant worsening in Physician’s Global Assessment
• Post hoc exploratory analyses of BLISS-76 data at Weeks 52 and 76 evaluated SRI response using greater SELENA SLEDAI reductions (-5, -6, -7, -8, -9 and -10 points) than the 4-point reduction used for the primary endpoint. Using these higher SELENA SLEDAI thresholds, a greater treatment effect was observed, with significant improvements in SRI response for the 10 mg/kg treatment group at both Week 52 and Week 76 (p<0.05 vs. placebo). New data will be presented at the International Congress on SLE from analyses of SRI response using SELENA SLEDAI reductions of -8, -9, and – 10 points (included below).  

	SRI Rate at Week 52			SRI Rate at Week 76
SELENA     SLEDAI	Placebo  N=275	1 mg/kg  N=271	10 mg/kg  N=273	Placebo  N=275	1 mg/kg  N=271	10 mg/kg  N=273
>4-point     reduction	33.5%	40.6%	43.2%*	32.4%	39.1%	38.5%
>5-point     reduction	20.4%	31.0%**	32.6%***	21.8%	28.4%	30.8%*
>6-point     reduction	18.9%	28.8%**	30.8%**	20.4%	26.9%	28.9%*
>7-point     reduction     N=649	13.4%	19.4%	21.3%*	13.9%	21.7%*	21.8%*
>8-point     reduction****     N=631	13.3%	18.5%	21.4%*	12.9%	19.9%*	21.9%**
>9-point     reduction****     N=440	8.2%	14.0%	15.4%	4.8%	14.7%**	15.4%**
>10-point     reduction****     N=420	8.6%	13.9%	15.4%	5.0%	14.6%**	14.0%*

 B-Cell Subsets

Belimumab acts by specifically recognizing, binding to, and inhibiting the biological activity of the naturally occurring protein BLyS (B-lymphocyte stimulator). In lupus and certain other autoimmune diseases, elevated levels of BLyS are believed to contribute to the production of autoantibodies – antibodies that attack and destroy the body’s own cells. The presence of autoantibodies appears to correlate with disease severity. In the BLISS-76 study, belimumab treatment resulted in selective and, vs. placebo, significantly greater median percent reductions in levels of B-cell and plasma B-cell subsets, with preservation of memory B-cells. The median percent changes from baseline included the following: 

• Greater reductions in CD20+ cells were observed at Week 8 in both belimumab treatment groups, reached statistical significance by Week 24 and increased through Week 52 and Week 76 (all p<0.0001 for both belimumab doses vs. placebo). 
• Significantly greater reductions in CD20+/CD27- naïve cells were observed at Week 8 in both belimumab treatment groups and increased through Weeks 24, 52 and 76 (all p<0.0001 for both belimumab doses vs. placebo). 
• Greater reductions in CD20+/CD69+ activated cells were observed at Week 24 in both belimumab treatment groups, reached statistical significance for belimumab 10 mg/kg by Week 52 which was maintained through Week 76, and reached significance for belimumab 1 mg/kg by Week 76 (all p<0.05 vs. placebo). 
• Greater reductions in CD20+/CD138+ plasmacytoid cells were observed at Week 8 in both belimumab treatment groups, reached statistical significance by Week 24 (p<0.05, vs. placebo), and increased or were maintained through Weeks 52 (p<0.001 vs. placebo) and 76 (p<0.001 and p<0.01 for belimumab 10 mg/kg and 1 mg/kg respectively vs. placebo). 
• A significantly greater reduction in CD20-/CD138+ plasma cells was observed at Week 8 in the belimumab 10 mg/kg group, which was maintained through Weeks 24, 52 and 76 (all p<0.01 vs. placebo). In the belimumab 1 mg/kg group, the greater reduction reached statistical significance by Week 24 (p<0.05 vs. placebo); however, statistical significance for the lower dose was not maintained through Weeks 52 and 76). 
• A significantly greater reduction in CD20-/CD27BR short-lived plasma cells was observed at Week 8 in the belimumab 10 mg/kg group, which was maintained through Weeks 24, 52 and 76 (all p<0.01 vs. placebo). Greater reductions were also observed In the belimumab 1 mg/kg group, but the difference did not reach statistical significance. 
• A significantly greater reduction in CD19+/CD27 BR/CD38BR SLE subset cells was observed at Week 8 in the belimumab 10 mg/kg group (p<0.01 vs. placebo), which was maintained through Weeks 24, 52 and 76 (all p<0.001 vs. placebo). Greater reductions were also observed In the belimumab 1 mg/kg group, but the difference did not reach statistical significance. 
• Significantly greater increases in CD20+/CD27+ memory cells were observed at Week 8 in both belimumab treatment groups and increased through Weeks 24, 52 and 76 (p<0.0001 at Weeks 8, 24 and 52, and p<0.05 at Week 76 for belimumab 10 mg/kg vs. placebo).

Effect on Protective Immune Response 

• Belimumab did not significantly affect the ability of SLE patients to maintain a protective response to pneumococcal, tetanus and influenza vaccines, which is consistent with the preservation of memory B-cells.

Safety

• In BLISS-76 through 76 weeks, belimumab was generally well tolerated, with rates of adverse events overall, serious and/or severe adverse events, all infections, serious and/or severe infections, and discontinuations due to adverse events comparable between treatment groups receiving belimumab plus standard of care and the treatment group receiving placebo plus standard of care. Serious and/or severe adverse events were reported in 29.0% of patients on belimumab and 26.2% of patients on placebo. Infections were reported in 74.3% of patients on belimumab and 69.1% of patients on placebo. Serious and/or severe infections were reported in 7.7% of patients on belimumab and 8.4% of patients on placebo. Serious and/or severe infusion reactions were reported in 1.1% of patients on belimumab and 0.7% of patients on placebo. Discontinuations due to adverse events were 7.5% in the belimumab treatment groups and 8.4% in the placebo treatment group. A total of seven malignancies were reported in BLISS-76: 2, 4, and 1 in the belimumab 10 mg/kg, belimumab 1 mg/kg and placebo groups, respectively. A total of three deaths were reported in the study: 1, 2, and 0 in the belimumab 10 mg/kg, belimumab 1 mg/kg and placebo groups, respectively.

About the BENLYSTA (belimumab) Phase 3 Development Program

The Phase 3 development program for belimumab included two double-blind, placebo-controlled, multi-center Phase 3 superiority trials – BLISS-52 and BLISS-76 – to evaluate the efficacy and safety of belimumab plus standard of care, versus placebo plus standard of care, in seropositive (HEp-2 ANA > 1:80 and/or anti-dsDNA > 30 IU/mL) patients with SLE. Both BLISS-52 and BLISS-76 have now been completed. This is the largest clinical trial program ever conducted in lupus patients. BLISS-52 randomized and treated 865 patients at 90 clinical sites in 13 countries, primarily in Asia, South America and Eastern Europe. BLISS-76 randomized and treated 819 patients at 136 clinical sites in 19 countries, primarily in North America and Europe.

The design of the two trials was similar, but the duration of therapy in the two studies was different – 52 weeks for BLISS-52 and 76 weeks for BLISS-76. The data from the BLISS-76 Phase 3 study were analyzed after 52 weeks in accord with the study protocol, in support of the BLA and MAA submissions. The BLISS-76 study then continued for an additional 24 weeks through the full 76-week treatment period, with the objective of generating additional information about belimumab based on a variety of secondary endpoints. HGS designed the Phase 3 program for belimumab in collaboration with GSK and leading international SLE experts, and the program is being conducted under a Special Protocol Assessment agreement with FDA.

About BENLYSTA (belimumab)

Belimumab is an investigational human monoclonal antibody drug that specifically recognizes and inhibits the biological activity of B-lymphocyte stimulator, or BLyS. BLyS is a naturally occurring protein discovered by HGS that is required for the development of B-lymphocyte cells into mature plasma B cells. Plasma B cells produce antibodies, the body’s first line of defense against infection. In lupus and certain other autoimmune diseases, elevated levels of BLyS are believed to contribute to the production of autoantibodies – antibodies that attack and destroy the body’s own healthy tissues. The presence of autoantibodies appears to correlate with disease severity. Preclinical and clinical studies suggest that belimumab can reduce autoantibody levels in SLE. The results of two pivotal Phase 3 trials, BLISS-52 and BLISS-76, suggest that belimumab can reduce SLE disease activity.

In June 2010, GSK submitted a Marketing Authorization Application to the European Medicines Agency, seeking approval to market belimumab in Europe for treatment of autoantibody-positive patients with SLE, and HGS submitted a Biologics License Application (BLA) to the U.S. Food and Drug Administration seeking approval to market belimumab in the United States. No new drug for lupus has been approved by regulatory authorities in more than 50 years.

About the Collaboration with GlaxoSmithKline PLC (GSK)

In 2006, HGS and GSK entered into a definitive co-development and commercialization agreement under which HGS is conducting the belimumab Phase 3 trials, with assistance from GSK. The companies will share equally in Phase 3/4 development costs, sales and marketing expenses, and profits of any product commercialized under the agreement.

About Systemic Lupus Erythematosus

Systemic lupus erythematosus (SLE) is a chronic, life-threatening autoimmune disease. Approximately five million people worldwide, including approximately 1.5 million in the United States, suffer from various forms of lupus, including SLE. Lupus can occur at any age, but appears mostly in young people ages 15 to 45. About 90 percent of those diagnosed with lupus are women. African-American women are about three times more likely to develop lupus, and it is also more common in Hispanic, Asian and American Indian women. Symptoms may include extreme fatigue, painful and swollen joints, unexplained fever, skin rash and kidney problems. Lupus can lead to arthritis, kidney failure, heart and lung inflammation, central nervous system abnormalities, inflammation of the blood vessels and blood disorders. No new drug for lupus has been approved by regulatory authorities in more than 50 years. For more information on lupus, visit the Lupus Foundation of America at www.lupus.org, the Lupus Research Institute at www.lupusresearchinstitute.org, the National Institute of Arthritis and Musculoskeletal and Skin Diseases at www.niams.nih.gov, or Lupus Europe at www.lupus-europe.org.

About Human Genome Sciences

The mission of HGS is to apply great science and great medicine to bring innovative drugs to patients with unmet medical needs. The HGS clinical development pipeline includes novel drugs to treat lupus, inhalation anthrax, hepatitis C and cancer.

For more information about HGS, please visit the Company’s web site at www.hgsi.com. Health professionals and patients interested in clinical trials of HGS products may inquire via e-mail to medinfo@hgsi.com This e-mail address is being protected from spam bots, you need JavaScript enabled to view it or by calling HGS at (877) 822-8472.

HGS, Human Genome Sciences and BENLYSTA are trademarks of Human Genome Sciences, Inc. Other trademarks referenced are the property of their respective owners.

Safe Harbor Statement

This announcement contains forward-looking statements within the meaning of Section 27A of the Securities Act of 1933, as amended, and Section 21E of the Securities Exchange Act of 1934, as amended. The forward-looking statements are based on Human Genome Sciences’ current intent, belief and expectations. These statements are not guarantees of future performance and are subject to certain risks and uncertainties that are difficult to predict. Actual results may differ materially from these forward-looking statements because of Human Genome Sciences’ unproven business model, its dependence on new technologies, the uncertainty and timing of clinical trials and regulatory approvals, Human Genome Sciences’ ability to develop and commercialize products, its dependence on collaborators for services and revenue, its substantial indebtedness and lease obligations, its changing requirements and costs associated with facilities, intense competition, the uncertainty of patent and intellectual property protection, Human Genome Sciences’ dependence on key management and key suppliers, the uncertainty of regulation of products, the impact of future alliances or transactions and other risks described in the Company’s filings with the SEC. Existing and prospective investors are cautioned not to place undue reliance on these forward-looking statements, which speak only as of today’s date. Human Genome Sciences undertakes no obligation to update or revise the information contained in this announcement whether as a result of new information, future events or circumstances or otherwise.

Media Contact:
Jerry Parrott
Vice President, Corporate Communications
301-315-2777

Investor Contact:
Peter Vozzo
Senior Director, Investor Relations
301-251-6003