ROCKVILLE, Maryland -- October 28, 2003 -- Human Genome Sciences, Inc. (Nasdaq: HGSI) announced today that the results to date of clinical, preclinical and observational studies strongly support the ongoing clinical development of LymphoStat-B™ (a human monoclonal antibody to B-lymphocyte stimulator, BLyS™) for the treatment of systemic lupus erythematosus. The results were presented at the 67^th Annual Meeting of the American College of Rheumatology/Association of Rheumatology Health Professionals, which concludes today in Orlando, FL.

LymphoStat-B is a human monoclonal antibody that specifically recognizes and inhibits the biological activity of B-lymphocyte stimulator, or BLyS. BLyS is a naturally occurring protein discovered by Human Genome Sciences that is required for the development of B-lymphocyte cells into mature plasma B cells.¹ In lupus, rheumatoid arthritis, 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. Human Genome Sciences is developing LymphoStat-B as a potential treatment for lupus and rheumatoid arthritis. Patients with lupus currently are being dosed in a double-blind, placebo-controlled, multi-center Phase 2 clinical trial of LymphoStat-B.² LymphoStat-B has received a Fast Track Product designation from the U.S. Food and Drug Administration (FDA) for its potential use in treating systemic lupus erythematosus.³ The Company also plans to initiate a Phase 2 clinical trial of LymphoStat-B for treatment of rheumatoid arthritis.

A poster entitled Safety, Pharmacokinetic and Pharmacodynamic Results of a Phase 1 Single and Double Dose-Escalation Study of LymphoStat-B (Human Monoclonal Antibody to BLyS) in SLE Patients (Abstract # 922) described the results of a multi-center, double-blind, placebo-controlled, dose-escalation Phase 1 clinical trial designed to determine the safety and pharmacology of LymphoStat-B in adult patients with systemic lupus erythematosus.⁴ Seventy patients with mild to moderate disease activity who were receiving standard therapies were enrolled and randomized in the study. LymphoStat-B or placebo was administered intravenously at 1 milligram (mg)/kilogram (kg), 4 mg/kg, 10 mg/kg, or 20 mg/kg. Patients received either a placebo, a single dose of LymphoStat-B, or two doses of LymphoStat-B given twenty-one days apart. Safety was the primary endpoint of the study. The pharmacology of LymphoStat-B and biological markers of B-cell function also were evaluated.

Results show that LymphoStat-B is well tolerated with no clinically significant differences from placebo in adverse events or laboratory abnormalities. No drug-related serious adverse events were reported. The half-life of LymphoStat-B was shown to be between 13 and 17 days, which is consistent with that of other human monoclonal antibodies. A dose-proportional pharmacokinetic profile was observed. As expected based on preclinical research and LymphoStat-B's mechanism of action, results show that LymphoStat-B significantly reduces the levels of circulating B cells (CD 20⁺), the precursor cells to those that produce the body's normal and abnormal antibodies. In patients treated with LymphoStat-B, reductions in CD 20⁺ cells ranging from twelve percent to forty-seven percent compared to placebo were observed at the last visit, and at other time points after day 42 for single-dose cohorts and after day 49 for double-dose cohorts. In addition, significant reductions in anti-dsDNA (double-stranded DNA) autoantibody levels were observed in some LymphoStat-B treatment cohorts.

Richard Furie, M.D., a lead clinical trial investigator, Chief, Division of Rheumatology and Allergy Clinical Immunology, North Shore University Hospital, Manhasset, NY, and Associate Professor of Medicine, New York University School of Medicine, said, "The results of this initial clinical trial demonstrate that LymphoStat-B was well tolerated and biologically active. Lupus is a complex and often devastating chronic illness. Patients with lupus can experience any number of symptoms that can flare unexpectedly, including extreme fatigue, painful and swollen joints, unexplained fever, skin rash, and kidney problems. Only a limited number of treatment options are currently available to these patients. We are encouraged by the Phase 1 results and by the observational data that continue to emerge in support of the role of BLyS in autoimmune diseases such as lupus and rheumatoid arthritis."

An oral presentation entitled BLyS Plasma Concentrations Correlate with Disease Activity and Levels of Anti-dsDNA Autoantibodies and Immunoglobulins (IgG) in a SLE Patient Observational Study (Abstract #1712) described the interim results of a two-year observational study designed to evaluate longitudinally the relationship between BLyS plasma concentrations and SLE disease activity in patients receiving standard-of-care therapy.⁵ Two hundred and forty-five patients who met the American College of Rheumatology (ACR) criteria for systemic lupus erythematosus were enrolled in the study and seen in the clinic every 3-6 months and for acute care visits. The SELENA SLEDAI disease activity scale and anti-dsDNA autoantibody and plasma BLyS levels were assessed at each clinic visit. Immunoglobulin subtypes were assessed every 6 months. To date, patients have participated in the study for an average of 15 months. Interim results demonstrate that BLyS levels are positively and significantly associated with SELENA SLEDAI scores across all visits (p=0.016), IgG levels across all visits (p=0.002), and anti-dsDNA autoantibody levels in most visits (p<0.013). Seventy-eight percent of the patients had a greater than twenty-five percent change from their baseline BLyS levels on at least one visit throughout the study. Of those patients, thirty-six percent had a greater than fifty percent change from their baseline BLyS levels on at least one visit. Multivariate analysis showed that increases in SELENA SLEDAI score (worsening disease activity) from the previous visit to the current visit were associated with elevated BLyS levels in the previous visit (p=0.017). Increases in SELENA SLEDAI score from the previous visit to the current visit also were correlated with increases in BLyS levels during that time period (p=0.0154).

Michelle Petri, M.D., M.P.H., lead author, Professor of Medicine, Division of Molecular and Clinical Rheumatology, and Director of the Lupus Center, The Johns Hopkins Hospital, Baltimore, MD, said, "Preliminary results of this observational study show that elevated BLyS levels in patients with lupus are positively and significantly correlated with increased disease activity, as well as increased autoantibody and immunoglobulin levels. Furthermore, changes in the SELENA SLEDAI disease activity scale from previous to current visit are positively associated with BLyS levels in the previous visit and with changes in BLyS levels, suggesting that BLyS levels may be a biomarker of current and future disease activity. We look forward to continuing our evaluation of the potential contributory role that BLyS may have in lupus disease activity and progression."

A poster entitled Effects of LymphoStat-B, a BLyS Antagonist, When Administered Intravenously to Cynomolgus Monkeys (Abstract # 1537) described the results of a preclinical study designed to evaluate the tolerability and effects of LymphoStat-B administered in cynomolgus monkeys by intravenous injection every two weeks for 13 or 26 weeks.⁶ LymphoStat-B was administered at doses of 5, 15 or 50 mg/kg. Safety and pharmacology endpoints were measured at 3 and 6 months and after an 8-month treatment-free period. Results show that LymphoStat-B is well tolerated and biologically active at the doses administered. Despite decreases in B-lymphocytes, monkeys treated with LymphoStat-B had no increase in infections. Exposure to LymphoStat-B increased with dose and extended into the recovery period. Data show that LymphoStat-B significantly reduces circulating B cells (CD20⁺) and mature B cells (CD20⁺/CD21⁺), as well as B cells in the lymphoid tissue. The treatment-related effects of LymphoStat-B were reversible within the 8-month treatment-free period.

David C. Stump, M.D., Senior Vice President, Drug Development, said, "Results from the clinical, preclinical and observational studies presented this week demonstrate that LymphoStat-B is well tolerated and biologically active, and strongly support our advancement of LymphoStat-B into Phase 2 clinical development for the treatment of lupus and other autoimmune diseases. We have begun to dose patients in our ongoing Phase 2 study of LymphoStat-B for the treatment of systemic lupus erythematosus. In addition, we plan soon to initiate a Phase 2 study of LymphoStat-B in patients with rheumatoid arthritis. We look forward to the progress of these clinical trials, and to further definition of LymphoStat-B's therapeutic potential."

Craig A. Rosen, Ph.D., President, Research and Development, said, "Hundreds of thousands of people are afflicted with systemic lupus erythematosus in the United States alone. The majority are young women, between the ages of fifteen and forty-five. Worldwide, millions of people suffer from lupus and other autoimmune diseases such as rheumatoid arthritis. We believe that LymphoStat-B, by neutralizing the effects of BLyS, may offer a much-needed new approach to treating such diseases."

LymphoStat-B is a human monoclonal antibody that specifically recognizes and inhibits the biological activity of B-lymphocyte stimulator, or BLyS. BLyS is a naturally occurring protein discovered by Human Genome Sciences that is required for the development of B-lymphocyte cells into mature plasma B cells.¹ Plasma B cells produce antibodies, the body's first line of defense against infection. Laboratory studies have indicated that higher than normal levels of BLyS may contribute to the pathogenesis of autoimmune diseases, such as systemic lupus erythematosus and rheumatoid arthritis.^{7, 8, 9, 10} Autoimmune diseases are diseases in which the body is attacked by its own immune system.

Retrospective and prospective studies have shown elevated levels of BLyS in the blood of many patients with systemic lupus erythematosus, and in the blood and joint fluid of patients with rheumatoid arthritis.^{5, 11, 12, 13, 14, 15} The results of prospective studies also now show a significant correlation of elevated levels of BLyS with systemic lupus erythematosus disease activity.⁵ LymphoStat-B acts by: (1) binding to BLyS, (2) inhibiting BLyS's stimulation of B-cell development, and (3) restoring the potential for autoantibody-producing B cells to undergo the normal process of apoptosis (programmed cell death). In vitro and in vivo preclinical studies show that LymphoStat-B can reverse the immune stimulatory effects of BLyS.¹⁶

LymphoStat-B was made in a collaboration between Human Genome Sciences and Cambridge Antibody Technology. The drug will be manufactured in Human Genome Sciences' manufacturing facility, located in Rockville, MD. Human Genome Sciences holds the commercial rights to the drug.

For more information on LymphoStat-B, see www.hgsi.com/products/LSB.html. For more information about lupus, rheumatoid arthritis, or autoimmune diseases, visit The Lupus Foundation at www.lupus.org, the Arthritis Foundation at www.arthritis.org, or the National Institute of Arthritis and Musculoskeletal and Skin Diseases at www.niams.nih.gov. For more information about the FDA's Fast Track Drug Development Programs, see www.fda.gov.

For additional information on Human Genome Sciences, please visit our web site at www.hgsi.com.

Health professionals or patients interested in inquiring about LymphoStat-B trials or any other study involving HGSI products are encouraged to inquire via the Contact Us section of the Human Genome Sciences web site, www.hgsi.com/products/request.html, or by calling us at (301) 610-5790, extension 3550.

Human Genome Sciences is a company with the mission to treat and cure disease by bringing new gene-based drugs to patients.

HGS, Human Genome Sciences, BLyS and LymphoStat-B are trademarks of Human Genome Sciences, Inc.

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 the Company's unproven business model, its dependence on new technologies, the uncertainty and timing of clinical trials, the Company's 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 planned facilities, intense competition, the uncertainty of patent and intellectual property protection, the Company's 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 Securities and Exchange Commission. 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.

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Footnotes:

1. (HGSI Press Release) Human Genome Sciences Announces the Discovery of a Novel Immune Stimulant. July 8, 1999.

3. (HGSI Press Release) Results Of Phase 1 Clinical Trial Demonstrate That LymphoStat-B Is Safe And Biologically Active In Patients With Systemic Lupus Erythematosus. April 21, 2003.

4. Furie R, Stohl W, Ginzler E, et al. Safety, Pharmacokinetic and Pharmacodynamic Results of a Phase 1 Single and Double Dose-Escalation Study of LymphoStat-B (Human Monoclonal Antibody to BLyS) in SLE Patients. 67^th Annual Scientific Meeting of the American College of Rheumatology/Association of Rheumatology Health Professionals. October 26, 2003. Abstract 922.

5. Petri M, Stohl W, Chatham W, et al. BLyS Plasma Concentrations Correlate with Disease Activity and Levels of Anti-dsDNA Autoantibodies and Immunoglobulins (IgG) in a SLE Patient Observational Study. 67^th Annual Scientific Meeting of the American College of Rheumatology/Association of Rheumatology Health Professionals. October 27, 2003. Abstract #1712.

6. Halpern W, Lappin P, Zanardi T, et al. Effects of LymphoStat-B, a BLyS Antagonist, When Administered Intravenously to Cynomolgus Monkeys. 67^th Annual Scientific Meeting of the American College of Rheumatology/Association of Rheumatology Health Professionals. October 27, 2003. Abstract # 1537.

7. Gross JA, Johnston J, Mudri S, et al. TACI and BCMA are receptors for a TNF homologue implicated in B-cell autoimmune disease. Nature. 2000; 404: 995-999.

8. Khare S.D., Saarosi I, Xia XZ, et al. Severe B cell hyperplasia and autoimmune disease in TALL-1 transgenic mice. Proc Natl Acad Sci USA. 2000; 97: 3370-3375.

9. MacKay F., Woodcock SA, Lawton P, et al. Mice transgenic for BAFF develop lymphocytic disorders along with autoimmune manifestations. J. Exp. Med. 1999; 190: 1697-1710.

10. Wang H, Marsters SA, Baker T, et al. TACI-ligand interactions are required for T cell activation and collagen-induced arthritis in mice. Nature Immunol. 2001; 2: 632-637.

11. (HGSI Press Release) High Levels of BLyS Implicated in Lupus and Rheumatoid Arthritis Patients. October 30, 2000.

12. Zhang J, Roschke V, Baker K, et al. Cutting edge: A role for B lymphocyte stimulator in systemic lupus erythematosus. J Immuno. 2001; 166:6-10.

13. Cheema GS, Roschke V, Hilbert DM and Stohl W. Elevated Serum B Lymphocyte Stimulator Levels in Patients with Systemic Immune-Based Rheumatic Diseases. Arthritis & Rheumatism June 2001; 44(6): 1313-1319.

14. Carter RH. A role for BLyS in tissue inflammation? Arthritis & Rheumatism April 2003; 48(4): 882-885.

15. Tan S, Roschke V, Perry JW, et al. Local production of B lymphocyte stimulator and APRIL in arthritic joints of patients with inflammatory arthritis. Arthritis & Rheumatism April 2003; 48(4): 982-992.

16. Sekut L, Sturm B, Poortman C, et al. Characterization of a Human Monoclonal Antibody That Antagonizes B-Lymphocyte Stimulator Bioactivities. American College of Rheumatology 2001 Annual Meeting, Abstract 1377.

CONTACTS:
David C. Stump
Senior Vice President, Drug Development
301/309-8504
Jerry Parrott
Vice President, Corporate Communications
301/315-2777
Kate de Santis
Director, Investor Relations
301/251-6003