ROCKVILLE, Maryland – August 24, 2004 – Human Genome Sciences, Inc. (Nasdaq: HGSI) announced today that it has begun dosing patients in a Phase 1 clinical trial of HGS-TR2J, a novel agonistic human monoclonal antibody to TRAIL Receptor 2, in patients with advanced solid malignancies.

HGS-TR2J arises from a license agreement entered into at the end of 2002, under which Human Genome Sciences and the Pharmaceutical Division of Kirin Brewery Company, Ltd., agreed to collaborate on the development and commercialization of antibodies to TRAIL Receptor 2.1 Under the agreement, Kirin will develop and commercialize any resulting drug in Japan and Asia/Australasia, and Human Genome Sciences will develop and commercialize any resulting drug in North America, Europe , and the rest of the world.

The Phase 1 clinical trial of HGS-TR2J is an open-label dose-escalation study. The primary objectives of the clinical trial are to assess safety and tolerability. Pharmacokinetics and disease response also will be evaluated. The trial will be conducted in Canada, and will enroll a maximum of forty-eight patients with relapsed or refractory advanced solid malignancies who have failed standard therapies and for whom no curative option exists, or who have refused all other therapies.

Preclinical studies will be presented at several international cancer meetings this fall, which demonstrate that HGS-TR2J binds TRAIL Receptor 2 with high affinity, induces apoptosis and has anti-tumor activity, both as a single agent and in combination with chemotherapy. HGS-TR2J mimics the activity of native TRAIL (tumor necrosis factor-related apoptosis-inducing ligand) and, thus, is considered an agonistic antibody. Numerous nonclinical studies have shown that cell lines derived from a broad array of solid and hematological human tumors, including lung, colon, breast, multiple myeloma, prostate and pancreas, are sensitive to killing by apoptosis (programmed cell death) induced by native TRAIL or by agonistic antibodies to TRAIL Receptors 1 and 2.2-24 The results of in vitro and in vivo preclinical studies providing support for initiating clinical development of HGS-TR2J will be presented at the 16th EORTC-NCI-AACR Symposium on “Molecular Targets and Cancer Therapeutics” (Geneva, September 28-October 1, 2004)25, 26, and the 29th European Society of Medical Oncology Congress (October 29-November 2, 2004).27

Hal Hirte, M.D., Head, Medical Oncology and Systemic Therapy Program, Juravinski Cancer Centre, and Associate Professor, Department of Medicine, McMaster University (Hamilton, Ontario), said, “The ability of TRAIL and TRAIL receptor agonistic antibodies to trigger apoptosis in numerous cancer cell lines has been widely reported. HGS-TR2J is an agonistic antibody to TRAIL Receptor 2, and may offer certain therapeutic advantages in comparison to native TRAIL, due to its significantly longer circulating half-life and its exclusive specificity to TRAIL receptor 2. We look forward to exploring its potential in this initial clinical trial in cancer patients.”

Gilles Gallant, B. Pharm., Ph.D., Vice President, Clinical Oncology, said, “The results of preclinical studies to date demonstrate that agonistic TRAIL receptor antibodies, such as HGS-TR2J, are able to trigger cancer cell death through apoptosis in a number of tumor types.15-23 We believe that HGS-TR2J has significant potential for the treatment of a broad range of solid malignancies, either as a single agent or in combination with chemotherapy, and we are pleased to initiate its clinical development.”

Craig A. Rosen, Ph.D., President, Research and Development, said, “We are very pleased with the progress of our collaboration with Kirin. Our own preclinical studies, as well as those conducted by others, provide mounting evidence that agonistic antibodies to the death domain-containing TRAIL receptors have the potential to provide treatment options to patients with a broad range of tumor types. Our collaboration with Kirin affords us the opportunity to study the Kirin antibodies to TRAIL Receptor 2 alongside our own antibodies and to determine the optimal drug candidate to advance through clinical trials. Early this year, Human Genome Sciences set as a milestone the goal of entering 1-2 new drugs into clinical development in 2004. Entering HGS-TR2J into Phase 1 helps meet that milestone. As we continue to advance our clinical development program, we expect to maintain our priority focus on oncology and immunology/infectious disease.”

Human Genome Sciences originally identified the TRAIL Receptor 2 protein as a member of the tumor necrosis factor family of proteins. TRAIL Receptor 2 often is referred to as a “death receptor” because of its ability to cause apoptosis in tumor cells when triggered by the natural ligand TRAIL. HGS-TR2J was made in a collaboration with the Pharmaceutical Division of Kirin Brewery Company, Ltd. HGS-TR2J will be produced in the Human Genome Sciences clinical manufacturing facility located in Rockville, Maryland.

For more information on HGS-TR2J, see www.hgsi.com/products/tr2j. Health professionals or patients interested in inquiring about clinical trial 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. For additional information on Human Genome Sciences, please visit our web site at www.hgsi.com.

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

HGS and Human Genome Sciences 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 Joint Development Of Antibody For The Treatment Of Cancer With Kirin. December 3, 2002.
2. Apo-2L/TRAIL in Cytokine Reference. Ashkenazi A. Academic Press; 2000.
3. Safety and anti-tumor activity of recombinant soluble APO2 ligand. Ashkenazi A, Pai RC, Fong S, et al. Journal of Clinical Investigation. 1999; 104: 155-162.
4. The receptor for the cytotoxic ligand TRAIL. Pan G, et al. Science 1997; 276: 111-113.
5. Tumor necrosis factor-related apoptosis-inducing ligand induces caspase-dependent interleukin-8 expression and apoptosis in human astroglioma cells. Choi C, Kutsch O, Pak J, et al. Molecular and Cellular Biology 2002; 22:724-736.
6. Tumor necrosis factor-related apoptosis-inducing ligand’s antitumor activity in vivo is enhanced by the chemotherapeutic agent CPT-11. Gliniak B, Le T. Cancer Research 1999; 59:6153-6158.
7. Preclinical studies to predict the disposition of Apo2L/tumor necrosis factor-related apoptosis-inducing ligand in humans: Characterization of in vivo efficacy, pharmacokinetics, and safety. Kelley SK, et al. J. Pharmacol. Exp. Ther. 2001; 299:31-38.
8. TRAIL/Apo2L ligand selectively induces apoptosis and overcomes drug resistance in multiple myeloma: Therapeutic applications. Mitsiades N, Treon SP, Mitsiades N, et al. Blood 2001; 98:795-804.
9. Induction of apoptosis by Apo-2 Ligand, a new member of the tumor necrosis factor receptor family. Pitti RM, Marsters SA, Ruppert S, et al. J. Biol. Chem. 1996; 271:12690-12697.
10. Expression and antitumor effects of TRAIL in human cholangiocarcinoma. Tanaka S, Sugimachi K, Shirabe K, et al. Hepatology 2000; 32:523-527.
11. Increased death receptor 5 expression by chemotherapeutic agents in human gliomas causes synergistic cytotoxicity with tumor necrosis factor-related apoptosis-inducing ligand in vitro and in vivo. Nagane M, Pan G, Weddle JJ, et al. Cancer Research 2000; 60:847-853.
12. Tumoricidal activity of tumor necrosis factor-related apoptosis-inducing ligand in vivo. Walczak H, Miller RE, Ariail K, et al. Nat. Med. 1999; 5:157-163.
13. Identification and characterization of a new member of the TNF family that induces apoptosis. Wiley SR, Schooley K, Smolak PJ, et al. Immunity 1995; 3:673-682.
14. Apoptosis induced in normal human hepatocytes by tumor necrosis factor-related apoptosis-inducing ligand. Jo M, et al. Nat. Med. 2000; 6:564-567.
15. Differential hepatocyte toxicity of recombinant Apo2L/TRAIL versions. Lawrence D, Shahrokh Z, Marsters S, et al. Nat. Med. 2001; 7:383-385.
16. Selective Agonistic Monoclonal Antibodies to the TRAIL Receptors R1 and R2 Induce Cell Death and Potentiate the Effect of Chemotherapy and Bortezomib in Primary and Cultured Lymphoma Cells. G.V. Georgakis, et al. American Society of Clinical Oncology Annual Meeting, 2004: Abstract #6595.
17. TRAIL R2-mAb, a human agonistic monoclonal antibody to tumor necrosis factor-related apoptosis inducing ligand receptor 2, affects tumor growth and induces apoptosis in human tumor xenograft models in vivo. Robin C. Humphreys, Ralph F. Alderson, Eliel Bayever, Kevin Connolly, Gil H. Choi, Norma Lynn Fox, Gilles Gallant, Krzystof J. Grzegorzewski, Viktor Roschke, Theodora W. Salcedo, Jing Zhang, Junli Zhang, Vivian R. Albert. 94th AACR Annual Meeting. Abstract 642.
18. TRAIL-R2 mAb, a human agonistic monoclonal antibody to tumor necrosis factor-related apoptosis inducing ligand receptor 2, induces apoptosis in human tumor cells. Ralph F. Alderson, Charles E. Birse, Kevin Connolly, Gil H. Choi, Norma Lynn Fox, Gilles Gallant, Ina Han, Robin C. Humphreys, Ron Johnson, Palanisamy Kanakaraj, Vikram Patel, Oxana Pickeral, Laurie Pukac, Viktor Roschke, Theodora Salcedo, Tara Shah, Junli Zhang, Vivian R. Albert. 94th AACR Annual Meeting. Abstract 963.
19. TRM-1, a fully human TRAIL-R1 agonistic monoclonal antibody, displays in vitro and in vivo anti-tumor activity. Salcedo, Alderson, Basu, et al. American Association for Cancer Research 93rd Annual Meeting. April 2002, Abstract 4240.
20. TRAIL-R1 mAb, a human agonistic monoclonal antibody to tumor necrosis factor-related apoptosis-inducing ligand receptor 1, induces apoptosis in human tumor cells in vitro and in vivo. Pukac, Kanakaraj, Alderson, et al. American Association for Cancer Research 94th Annual Meeting. July 2003, Abstract 6429.
21. TRAIL-R1 and TRAIL-R2 Human Agonistic Monoclonal Antibodies Display In Vitro and In Vivo Activity on Human Cancer Cells. Humphreys R, et al. Society for Biological Therapy 2002; oral presentation.
22. Isotype-dependent inhibition of tumor growth in vivo by monoclonal antibodies to death receptor 4. Chuntharapai A, Dodge K, Grimmer K, et al. J. Immunol. 2001; 166:4891-4898.
23. Tumoricidal activity of a novel anti-human DR5 monoclonal antibody without hepatocyte cytotoxicity. Ichikawa K, Liu W, Zhao L, et al. Nat. Med. 2001; 7:954-960.
24. TRM-1, a fully human TRAIL-R1 agonistic monoclonal antibody, displays in vitro and in vivo anti-tumor activity. Salcedo, Alderson, Basu, et al. American Association for Cancer Research 93rd Annual Meeting. April 2002, Abstract 4240.
25. HGS-TR2J, a human, agonistic, TRAIL receptor 2 monoclonal antibody, induces apoptosis, tumor regression and growth inhibition as a single agent in diverse human solid tumor cell lines. Humphreys R, et al. EORTC-NCI-AACR symposium on Molecular Targets and Cancer Therapeutics, 2004: Poster to be presented September 29, 2004.
26. Enhanced apoptosis and tumor regression induced by a direct agonist antibody to TRAIL-R2. Kataoka S, et al. EORTC-NCI-AACR symposium on Molecular Targets and Cancer Therapeutics, 2004: Poster to be presented September 30, 2004.
27. HGS-TR2J, a human, agonistic, TRAIL receptor 2 monoclonal antibody, induces apoptosis in vitro, in vivo tumor regression and growth inhibition in several human tumor cell lines and enhances the anti-tumor activity of platinum and taxane agents in lung and ovarian tumor cell lines. Robin C. Humphreys et al 29th ESMO Congress (poster symposium to be presented Nov 1) 29 October - 2 November 2004 Vienna, Austria.

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