ROCKVILLE, Maryland – March 3, 2005 – Human Genome Sciences, Inc. (Nasdaq: HGSI) announced today that it has completed the enrollment and initial dosing of patients in a Phase 2 clinical trial of HGS-ETR1 (mapatumumab) in advanced non-Hodgkin’s lymphoma.

The Phase 2 clinical trial is a multi-center, open-label study to evaluate the efficacy, safety and tolerability of HGS-ETR1, an agonistic human monoclonal antibody to TRAIL receptor 1, in patients with relapsed or refractory non-Hodgkin’s lymphoma. Patients enrolled in the trial are receiving up to six cycles of treatment in the absence of disease progression, with HGS-ETR1 administered as an intravenous infusion once every twenty-one days. The objectives of the study are to evaluate disease activity and tumor response to HGS-ETR1 in patients with advanced non-Hodgkin’s lymphoma, to evaluate the safety and tolerability of HGS-ETR1, and to determine plasma concentrations of HGS-ETR1 for use in a population pharmacokinetic analysis.

On November 30, 2004, Human Genome Sciences announced the completion of enrollment and initial dosing of patients in a Phase 2 study of HGS-ETR1 in advanced non-small cell lung cancer.¹ On February 23, 2005, the company announced the completion of enrollment and initial dosing of a Phase 2 study of the drug in advanced colorectal cancer.² The three Phase 2 studies of HGS-ETR1 initiated to date fit into a global clinical development program through which Human Genome Sciences is evaluating the novel, genomics-derived anticancer drug’s potential for use in the treatment of specific cancers.

Anas Younes, M.D., Professor, Lymphoma/Myeloma, University of Texas M.D. Anderson Cancer Center, Houston, said, “The current standard of care for non-Hodgkin’s lymphoma calls for treating most patients with a combination of chemotherapy and, in recent years, monoclonal antibodies. This therapeutic approach produces cures in approximately fifty percent of patients with aggressive lymphoma. Additional chemotherapeutic and other therapeutic modalities are used to treat non-Hodgkin’s lymphoma patients who relapse or do not respond, but cures are difficult to achieve. There remains a significant need for new therapies that can improve response rates, extend the duration of response, extend survival, minimize toxicity, and provide patients with improved quality of life. We look forward to continuing the evaluation of HGS-ETR1 to determine whether it may play a role in the treatment of non-Hodgkin’s lymphoma.” ^3-12

Gilles Gallant, B. Pharm., Ph.D., Vice President, Clinical Oncology, said, “We are pleased to have completed the enrollment and initial dosing of three Phase 2 studies to evaluate the potential use of HGS-ETR1 as a treatment for specific cancers, including non-small cell lung cancer, colorectal cancer and, now, non-Hodgkin’s lymphoma. We have seen a high level of interest in the emerging clinical and preclinical evidence demonstrating that agonistic antibodies to TRAIL receptors 1 and 2 have significant potential to provide novel therapeutic options to patients with a variety of cancer types, including non-Hodgkin’s lymphoma.^13-51 We expect to have the results of all three of the ongoing Phase 2 studies of HGS-ETR1 available in 2005. We also have initiated Phase 1b clinical studies of HGS-ETR1 in combination with chemotherapy. We plan to continue to elucidate the potential of HGS-ETR1 as a treatment for non-Hodgkin’s lymphoma and solid tumor malignancies, both as a single agent and in combination with chemotherapeutic agents.”

Interim results of two ongoing Phase 1 multi-center, open-label, dose-escalation clinical trials of HGS-ETR1 were presented in September 2004 at the 16 th EORTC-NCI-AACR Symposium on Molecular Targets and Cancer Therapeutics in Geneva, Switzerland.^13-15 The data presented demonstrate the safety and tolerability of HGS-ETR1 in patients with advanced solid tumors or non-Hodgkin’s lymphoma, and support further evaluation of HGS-ETR1 in Phase 2 clinical trials, both as a single agent and in combination with chemotherapy. Data were presented on 39 patients treated to date in a Phase 1 study conducted in patients with advanced solid tumors. Interim results of the ongoing study demonstrate that HGS-ETR1 can be administered safely and repetitively to patients with advanced solid malignancies at doses up to and including 10 mg/kg intravenously every 28 days. Some preliminary evidence of biological activity has been observed. Durable stable disease was observed in some patients. Data also were presented on 24 patients treated to date in an additional Phase 1 study conducted in patients with advanced solid tumors or non-Hodgkin’s lymphoma. Results presented from the ongoing clinical trial demonstrate that HGS-ETR1 is well tolerated with no clearly attributable toxicities to date and that the Maximum Tolerated Dose has not been reached. Stable disease has been observed in eight patients for greater than two cycles. The trial continues to enroll patients.

Human Genome Sciences, using genomic techniques, originally identified the TRAIL receptor-1 protein as a member of the tumor necrosis factor receptor super-family. The company’s own studies, as well as those conducted by others, show that TRAIL receptor 1 plays a key role in triggering apoptosis, or programmed cell death, in tumors. Human Genome Sciences took the approach of developing human monoclonal antibodies that would bind the receptor and stimulate the TRAIL receptor-1 protein to trigger apoptosis in cancer cells, in much the same way that the native TRAIL ligand (tumor necrosis factor-related apoptosis-inducing ligand) triggers it, but with the advantage of a longer half-life and an exclusive specificity for TRAIL receptor 1. The TRAIL receptor 1 agonistic human monoclonal antibody, HGS-ETR1, was made in a collaboration between Human Genome Sciences and Cambridge Antibody Technology.⁵² The drug will be produced in the Human Genome Sciences clinical manufacturing facilities located in Rockville, Maryland. Human Genome Sciences holds the commercial rights to the drug.

Non-Hodgkin’s lymphoma is the seventh most common cancer in the United States, with approximately 56,000 new cases diagnosed each year.⁵³

For more information about HGS-ETR1, see www.hgsi.com/products/ETR1.html. Health professionals interested in more information about trials involving Human Genome Sciences 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 (301) 610-5790, extension 3550.

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.

1. (HGSI Press Release) Human Genome Sciences Completes Patient Enrollment in a Phase 2 Clinical Trial of HGS-ETR1 for the Treatment of Non-Small Cell Lung Cancer. November 30, 2004.
2. (HGSI Press Release) Human Genome Sciences Completes Patient Enrollment in a Phase 2 Clinical Trial of HGS-ETR1 for the Treatment of Colorectal Cancer. February 23, 2005.
3. Coiffier B. Immunotherapy: The new standard in aggressive non-Hodgkin’s lymphoma in elderly. Semin Oncol 2003;30:21-27.
4. Coiffier B, Pfreundschuh M, Stahel R, et al. Aggressive lymphoma: Improving treatment outcome with rituximab. Anticancer Drugs 2002;13 (Suppl2):43-50.
5. Vose JM, Link BK, Grossbard ML, et al. Phase II study of rituximab in combination with CHOP chemotherapy in patients with previously untreated aggressive non-Hodgkin’s lymphoma. J Clin Oncol 2001;19:389-397.
6. Horning SJ, Cascoyne RD, Fischer RI. Large cell lymphoma; let’s chop down barriers to progress. ASCO Educational Book, Spring 1999;319-331.
7. McLaughlin P, Grillo-Lopez AJ, Link BK, et al. Rituximab chimeric anti-CD20 monoclonal antibody therapy for relapsed indolent lymphoma; half of patients respond to a four-dose treatment program. J Clin Oncol 1998;16:2825-2833.
8. Johnson PWM, Roahtimer AZS, Whelan JS, et al. Patterns of survival in patients with recurrent follicular lymphoma: A 20-year study from a single center. J Clin Oncol 1995;13:140-147.
9. Kimby E, Bjorkholm M, Gahrton G, et al. Clorambucil/prednisone vs. CHOP in symptomatic low-grade non-Hodgkin’s lymphomas; a randomized trial from Lymphoma Group of Central Sweden. Ann Oncol 1994;5(suppl):67-71.
10. Armitage JO. Treatment of non-Hodgkin’s lymphomas. N Engl J Med 1993;328:1023-1030.
11. Dana BW, Dahlberg S, Nathwanmi BN, et al. Long-term follow-up of patients with low-grade malignant lymphomas treated with doxorubicin-based chemotherapy or chemoimmunotherapy. J Clin Oncol 1993;11:644-651.
12. Cohen RB, et al. A Phase 1 clinical trial of HGS-ETR1, an agonistic monoclonal antibody to TRAIL-R1, in patients with advanced solid tumors.” 16^th EORTC-NCI-AACR Symposium on Molecular Targets and Cancer Therapeutics, 2004: Oral Presentation.
13. Hotte SJ, et al. Phase 1 study of a fully human monoclonal antibody to the tumor necrosis factor-related apoptosis-inducing ligand receptor 1 (TRAIL-R1) in subjects with advanced solid malignancies or non-Hodgkin’s lymphoma (NHL). 16^th EORTC-NCI-AACR Symposium on Molecular Targets and Cancer Therapeutics, 2004: Abstract #208.
14. (HGSI Press Release) Human Genome Sciences Reports Results of Ongoing Phase 1 Clinical Trials of HGS-ETR1 in Patients with Advanced Cancers. September 29, 2004.
15. Tolcher AW, et al. A Phase 1 and pharmacokinetic study of HGS-ETR1, a fully human monoclonal antibody to TRAIL-R1 (TRM-1), in patients with advanced solid tumors. American Society of Clinical Oncology Annual Meeting, 2004: Abstract #3060.
16. Le LH, et al. Phase 1 study of a fully human monoclonal antibody to the tumor necrosis factor-related apoptosis-inducting ligand Death Receptor 4 (TRAIL-R1) in subjects with advanced solid malignancies or non-Hodgkin’s lymphoma. American Society of Clinical Oncology Annual Meeting, 2004: Abstract #2533.
17. (HGSI Press Release) Human Genome Sciences Reports Results of Phase 1 Clinical Trials of HGS-ETR1 (TRAIL-R1 mAb) in Patients with Advanced Cancers. June 7, 2004.
18. Halpern W, et al. Variable distribution of TRAIL Receptor 1 in primary human tumor and normal tissues. 16 th EORTC-NCI-AACR Symposium on Molecular Targets and Cancer Therapeutics, 2004: Abstract #225.
19. Humphreys R, et al. 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. 16 th EORTC-NCI-AACR Symposium on Molecular Targets and Cancer Therapeutics, 2004: Abstract #204.
20. (HGSI Press Release) Human Genome Sciences Reports Results of Preclinical Studies of TRAIL-R1 and TRAIL-R2 Agonistic Human Monoclonal Antibodies at EORTC-NCI-AACR Symposium. October 1, 2004.
21. Younes A, Kadin ME. Emerging applications for the tumor necrosis factor family of ligands and receptors in cancer therapy. J Clin Oncol 2003;21:3526-3534.
22. Georgakis GV, Li Y, Humphreys R, et al. Activity of selective agonistic antibodies to TRAIL death receptors R1 and R2 in primary and cultured tumor cells of hematologic origin. Blood 2003;102:228a (abstract #799).
23. Johnson RL, Huang X, Fiscella M. Human agonistic anti-TRAIL antibodies, HGS-ETR1 and HGS-ETR2, induce apoptosis in diverse hematological tumor lines. Blood 2003;102:981a (abstract #3316).
24. Pukac L, Kanakaraj P, Alderson R, et al. 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. American Association for Cancer Research 94th Annual Meeting. July 2003, Abstract 6429.
25. Salcedo, Alderson R, Basu, et al. TRM-1, a fully human TRAIL-R1 agonistic monoclonal antibody, displays in vitro and in vivo anti-tumor activity. American Association for Cancer Research 93rd Annual Meeting. April 2002, Abstract #4240.
26. Humphreys R, et al. TRAIL-R1 and TRAIL-R2 human agonistic monoclonal antibodies display invitro and invivo activity on human cancer cells. Society for Biological Therapy 2002; oral presentation.
27. Ashkenazi A. Targeting death and decoy receptors of the tumor necrosis factor superfamily. Nat Revs Cancer 2002; 2:420-430.
28. Choi C, Kutsch O, Park J, et al. Tumor necrosis factor-related apoptosis-inducing ligand induces caspase-dependent interleukin-8 expression and apoptosis in human astroglioma cells. Mol Cell Biol 2002;22(3):724-736.
29. Chuntharapai A, Dodge K, Grimmer K, et al. Isotype-dependent inhibition of tumor growth invivo by monoclonal antibodies to death receptor 4. J Immunol 2001; 166:4891-4898.
30. Ichikawa K, Liu W, Zhao L, et al. Tumoricidal activity of a novel anti-human DR5 monoclonal antibody without hepatocyte cytotoxicity. Nat Med 2001;7:954-960.
31. Gores GJ, Kaufmann SH. Is TRAIL hepatoxic? Hepatology 2001;34:3-6.
32. Jo M, Kim TH, Seol DW, et al. Apoptosis induced in normal human hepatocytes by tumor necrosis factor-related apoptosis-inducing ligand. Nat Med 2000;6:564-567.
33. Kelley SK, Harris LA, Xie D, et al. 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. J Pharmacol Exp Ther 2001;299:31-38.
34. Lawrence D, Shahrokh Z, Marsters S, et al. Differential hepatocyte toxicity of recombinant ApoL/TRAIL versions. Nat Med 2001;7:383-385.
35. Mitsiades CS, Treon SP, Mitsiades N, et al. TRAIL/Apo2L ligand selectively induces apoptosis and overcomes drug resistance in multiple myeloma: Therapeutic applications. Blood 2001; 98:795-804.
36. Ashkenazi A. Apo-2L/TRAIL in cytokine reference. Academic Press 2000.
37. Tanaka S, Sugimachi K, Shirabe K, et al. Expression and antitumor effects of TRAIL in human cholangiocarcinoma. Hepatology 2000;32:523-527.
38. Ashkenazi A, Pai RC, Fong S, et al. Safety and anti-tumor activity of recombinant soluble Apo2 ligand. J Clin Invest 1999;104:155-162.
39. Walczak H, Miller RE, Ariail K, et al. Tumoricidal activity of tumor necrosis factor-related apoptosis-inducing ligand in vivo. Nat. Med. 1999; 5:157-163.
40. Snell V, Clodi K, Zhao S, et al. Activity of TNF-related apoptosis-inducing ligand (TRAIL) in haematological malignancies. Br J Haematol 1997;99:618-624.
41. Pitti RM, Marsters SA, Ruppert S, et al. Induction of apoptosis by Apo-2 ligand, a new member of the tumor necrosis factor receptor family. J Biol Chem. 1996; 271:12690-12697.
42. Wiley SR, Schooley K, Smolak PJ, et al. Identification and characterization of a new member of the TNF family that induces apoptosis. Immunity 1995;3:673-682.
43. Anderson KC, Bates MP, Slaughenhhoupt BL, et al. Expression of human B-cell associated antigens on leukemias and lymphomas: a model of human B-cell differentiation. Blood 1984;63:1424-1433.
44. Krishnan B, Ormerod MG, Kaye SB, Jackman AL. Effective combinations of carboplatin with low doses of TRAIL, HGS-ETR1 and HGS-ETR2 in the TRAIL-sensitive HX62 human ovarian tumour cell line. 16 th EORTC-NCI-AACR Symposium on Molecular Targets and Cancer Therapeutics, 2004: Abstract #637.
45. Georgakis GV, et al. 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. American Society of Clinical Oncology Annual Meeting, 2004: Abstract #6595.
46. Gillotte D, Zhang Y, Poortman C, et al. Human agonistic anti-TRAIL receptor antibodies, HGS-ETR1 and HGS-ETR2, induce apoptosis in ovarian tumor lines and their activity is enhanced by taxol and carboplatin. Proceedings from the AACR 2004; 73:3579.
47. Humphreys R, Shepard L, Zhang Y, et al. Novel, agonistic, human anti-TRAIL receptor monoclonal antibodies, HGS-ETR1 and HGS-ETR2, are capable of potently inducing tumor regression and growth inhibition as single agents and in combination with chemotherapeutic agents in models of human NSCLC. Proceedings of the AACR-NCI-EORTC International Conference on Molecular Targets and Cancer Therapeutics, Boston, November 2003.
48. Buchsbaum DJ, Zhou T, Grizzle WE, et al. Antitumor efficacy of TRA-8 anti-DR5 monoclonal antibody alone or in combination with chemotherapy and/or radiation therapy in a human breast cancer model. Clin Cancer Research 2003; 9:3731-3741.
49. Nagane M, Pan G, Weddle JJ, et al. Increased death receptor 5 expression by chemotherapeutic agents in human gliomas causes synergistic cytotoxicity with tumor necrosis factor-related apoptosis-inducing ligand invitro and invivo. Cancer Research. 2000; 60:847-853.
50. Gliniak B, Le T. Tumor necrosis factor-related apoptosis-inducing ligand’s antitumor activity invivo is enhanced by the chemotherapeutic agent CPT-11. Cancer Research 1999; 59:6153-6158.
51. (HGSI Press Release) Cambridge Antibody Technology and Human Genome Sciences Announce Second Drug Partnership. January 8, 2002.
52. Jemal A, Murray T, Samuels A, et al. Cancer statistics, 2003. CA Cancer J Clin. 2003;53:5-26.

CONTACT:
Jerry Parrott
Vice President, Corporate Communications
301/315-2777
Kate de Santis
Director, Investor Relations
301/251-6003