HUMAN GENOME SCIENCES BEGINS DOSING OF PATIENTS IN A PHASE 2 CLINICAL
TRIAL OF HGS-ETR1 IN NON-HODGKIN’S LYMPHOMA

- Clinical trial of novel genomics-derived anticancer drug is the third
Phase 2 study of the drug to be initiated in 2004 -

ROCKVILLE, Maryland – October 13, 2004 – Human Genome Sciences, Inc.
(Nasdaq: HGSI) announced today that it has begun dosing patients in a
Phase 2 clinical trial of HGS-ETR1 (agonistic human monoclonal antibody
to TRAIL Receptor 1) in patients with 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 in patients
with relapsed or refractory non-Hodgkin’s lymphoma. The Phase 2 study
will enroll a maximum of thirty patients. Each patient will receive 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. Disease response will be assessed using the
International Working Group Recommendations for Non-Hodgkin’s Lymphoma,
which were established in 1999 to provide an objective means for
evaluating changing disease status and the efficacy of drugs in the
treatment of non-Hodgkin’s lymphoma.1

In a separate press release distributed earlier today, Human Genome
Sciences announced that it has begin dosing patients in a Phase 2
clinical trial of HGS-ETR1 in patients with advanced colorectal cancer.2
On September 8, 2004, the company announced the initiation of a Phase 2
study of HGS-ETR1 in patients with advanced non-small cell lung cancer.3
The three Phase 2 studies of HGS-ETR1 initiated to date fit into a
global clinical development program through which Human Genome Sciences
plans to evaluate 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, “Non-Hodgkin’s lymphoma is the
seventh most common cancer in the United States, with approximately
56,000 new cases diagnosed each year. 4 The current standard of care
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. Those who relapse or do not respond are treated
with additional chemotherapeutic and other therapeutic modalities, but
cures are difficult to achieve. New therapies that can improve response
rates, extend the duration of response, extend survival, minimize
toxicity, and provide patients with improved quality of life represent a
significant need. We look forward to evaluating HGS-ETR1 to determine
whether it may play a role in the treatment of non-Hodgkin’s lymphoma.” 5-13

David C. Stump, M.D., Executive Vice President, Drug Development, said,
“The interim results from our ongoing Phase 1 clinical trials of
HGS-ETR1 demonstrate that it is well tolerated and can be safely and
repetitively administered to patients with non-Hodgkin’s lymphoma or
advanced solid tumors.14-19 Based on the clinical evidence to date,
along with strong preclinical support, we are pleased to initiate a
Phase 2 study of HGS-ETR1 in patients with non-Hodgkin’s lymphoma. We
look forward to continuing to elucidate the potential of HGS-ETR1 as a
treatment for solid tumor and other malignancies.”

Craig A. Rosen, Ph.D., President and Chief Operating Officer, said, “The
advancement of HGS-ETR1 to Phase 2 clinical trials is one of the key
milestones that we set for Human Genome Sciences at the beginning of
2004. We are now moving forward with a broad Phase 2 program of clinical
study to investigate the use of HGS-ETR1 in the treatment of specific
cancers, including colorectal cancer, non-small cell lung cancer, and
non-Hodgkin’s lymphoma. The results of our own in vitro and in vivo
preclinical studies, as well as studies conducted by others, demonstrate
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. 20-45 Our
preclinical studies also show that the activity of HGS-ETR1 may be
increased by co-treatment with chemotherapeutic agents.”46-52

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 16th EORTC-NCI-AACR Symposium on Molecular Targets and
Cancer Therapeutics in Geneva, Switzerland. 14-16 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
thirty-nine patients treated to date in a Phase 1 study conducted in
patients with advanced solid tumors.14, 16 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. No evidence of
drug-related hematologic or hepatic toxicity has been observed at the
doses administered to date. The Maximum Tolerated Dose (MTD) has not
been reached, and accrual in the trial continues at a dose of 10 mg/kg
every 14 days. Some preliminary evidence of biological activity has been
observed. Durable stable disease for greater than eight months was
observed in one patient with metastatic sarcoma. Durable stable disease
was observed for four months in one patient with head-and-neck cancer
and in one patient with Ewing’s sarcoma; both patients continue on
treatment. Data also were presented on twenty-four 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 MTD has not been
reached. Stable disease has been observed in eight patients for greater
than two cycles. The trial continues to enroll patients.15-16

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.53 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.

For more information about HGS-ETR1, see
www.hgsi.com/products/ETR1.html. Health professionals interested in more
information about trials 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 (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.

###

Footnotes:

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13, 2004.
3. (HGSI Press Release) Human Genome Sciences Advances Anti-Cancer Drug
to Phase 2 Clinical Development. September 8, 2004.
4. Jemal A, Murray T, Samuels A, et al. Cancer statistics, 2003. CA
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5. Coiffier B. Immunotherapy: The new standard in aggressive
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6. Coiffier B, Pfreundschuh M, Stahel R, et al. Aggressive lymphoma:
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7. Vose JM, Link BK, Grossbard ML, et al. Phase II study of rituximab in
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8. Horning SJ, Cascoyne RD, Fischer RI. Large cell lymphoma; let’s chop
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1993;328:1023-1030.
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1993;11:644-651.
14. 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.” 16th EORTC-NCI-AACR Symposium on Molecular Targets and Cancer
Therapeutics, 2004: Oral Presentation.
15. 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). 16th EORTC-NCI-AACR Symposium on Molecular
Targets and Cancer Therapeutics, 2004: Abstract #208.
16. (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.
17. 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.
18. 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.
19. (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.
20. Halpern W, et al. Variable distribution of TRAIL Receptor 1 in
primary human tumor and normal tissues. 16th EORTC-NCI-AACR Symposium on
Molecular Targets and Cancer Therapeutics, 2004: Abstract #225.
21. 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.
16th EORTC-NCI-AACR Symposium on Molecular Targets and Cancer
Therapeutics, 2004: Abstract #204.
22. (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.
23. 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.
24. 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).
25. 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).
26. 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.
27. 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.
28. Humphreys R, et al. TRAIL-R1 and TRAIL-R2 human agonistic monoclonal
antibodies display in vitro and in vivo activity on human cancer cells.
Society for Biological Therapy 2002; oral presentation.
29. Ashkenazi A. Targeting death and decoy receptors of the tumor
necrosis factor superfamily. Nat Revs Cancer 2002; 2:420-430.
30. 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.
31. Chuntharapai A, Dodge K, Grimmer K, et al. Isotype-dependent
inhibition of tumor growth in vivo by monoclonal antibodies to death
receptor 4. J Immunol 2001; 166:4891-4898.
32. 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.
33. Gores GJ, Kaufmann SH. Is TRAIL hepatoxic? Hepatology 2001;34:3-6.
34. 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.
35. 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.
36. Lawrence D, Shahrokh Z, Marsters S, et al. Differential hepatocyte
toxicity of recombinant ApoL/TRAIL versions. Nat Med 2001;7:383-385.
37. 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.
38. Ashkenazi A. Apo-2L/TRAIL in cytokine reference. Academic Press 2000.
39. Tanaka S, Sugimachi K, Shirabe K, et al. Expression and antitumor
effects of TRAIL in human cholangiocarcinoma. Hepatology 2000;32:523-527.
40. 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.
41. 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.
42. 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.
43. 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.
44. 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.
45. 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.
46. 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. 16th EORTC-NCI-AACR
Symposium on Molecular Targets and Cancer Therapeutics, 2004: Abstract #637.
47. 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.
48. 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.
49. 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.
50. 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.
51. 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 in vitro and in vivo. Cancer Research. 2000;
60:847-853.
52. Gliniak B, Le T. Tumor necrosis factor-related apoptosis-inducing
ligand’s antitumor activity in vivo is enhanced by the chemotherapeutic
agent CPT-11. Cancer Research 1999; 59:6153-6158.
53. (HGSI Press Release) Cambridge Antibody Technology and Human Genome
Sciences Announce Second Drug Partnership. January 8, 2002.

FOR IMMEDIATE RELEASE
CONTACTS:
David C. Stump, M.D.
Executive Vice President, Drug Development
240/314-4400
Jerry Parrott
Vice President, Corporate Communications
301/315-2777
Kate de Santis
Director, Investor Relations
301/251-6003

ARIAD INITIATES PHASE 2 CLINICAL TRIAL OF AP23573 IN PATIENTS WITH RELAPSED AND/OR REFRACTORY SARCOMAS

First global multicenter Phase 2 clinical trial of AP23573 in solid tumors

Cambridge, MA, September 30, 2004 - ARIAD Pharmaceuticals, Inc. (Nasdaq: ARIA) today announced initiation of enrollment of patients with bone and soft tissue sarcomas in the first multicenter Phase 2 clinical trial of its novel mTOR inhibitor, AP23573, as a single agent in solid tumors.

This non-randomized study will evaluate the clinical benefit of AP23573 in four well-defined groups of sarcoma patients, characterized by tumor type. Up to approximately 175 patients
will be enrolled in the trial at approximately 15 centers in the United States and Europe.AP23573 will be administered using a daily dosing regimen of drug.

"In our nearly completed Phase 1 clinical trials reported today at the EORTC international cancer symposium, all evaluable patients with relapsed and/or refractory sarcoma had evidence of anti-tumor activity - a promising result that supports our decision to further evaluate AP23573 in this patient population in Phase 2,"� said Harvey J. Berger, M.D., chairman and chief executive officer of ARIAD. "Despite advancements in anti-cancer therapy, currently available treatment options for such patients are extremely limited due the highly resistant
nature of this cancer. Sarcoma remains a disease with high unmet medical need."

The study will also include use of pharmacodynamic and pharmacogenomic biomarkers,including functional imaging, to assess the effects of AP23573 on the mTOR pathway and to
help identify patients who are likely to benefit most from treatment with AP23573.

About Sarcoma

Sarcomas are cancers of the connective tissue, including bones, muscles, fat, cartilage, and joints. Sarcomas can arise anywhere in the body and are divided into two main groups - bone tumors and soft tissue sarcomas. They are further sub-classified based on the type of cell found in the tumor. All sarcomas share certain pathologic characteristics. There are approximately 10,000 new cases of sarcoma diagnosed each year in the United States and close to 40,000 sarcoma patients being treated in the United States and Europe. More information about sarcomas is available on the web at http://www.sarcoma.net/facts.htm and at  http://www.sarcomafoundation.com/master.html?Articleld=90.

About AP23573

The small-molecule drug, AP23573, starves cancer cells and shrinks tumors by inhibiting the critical cell-signaling protein, mTOR, which regulates the response of tumor cells to nutrients and growth factors, and controls tumor blood supply and angiogenesis through effects on Vascular Endothelial Growth Factor (VEGF).

About ARIAD

ARIAD is engaged in the discovery and development of breakthrough medicines to treat cancer by regulating cell signaling with small molecules. The Company is developing a comprehensive approach to patients with cancer that addresses the greatest medical need - aggressive and advanced-stage cancers for which current treatments are inadequate. ARIAD also has an exclusive license to pioneering technology and patents related to certain NF-kB treatment methods, and the
discovery and development of drugs to regulate NF-kB cell-signaling activity, which may be useful in treating certain diseases. Additional information about ARIAD can be found on the web at http://www.ariad.com.

Some of the matters discussed herein are "forward-looking statements" within the meaning of the Private Securities Litigation Reform Act of 1995. Such statements are identified by the use of words such as "anticipate,"  "estimate,"� "expect,"  "project," "intend," "plan," "believe, " and other words and terms of similar meaning in connection with any discussion of future operating or financial performance. Such statements are based on management's current expectations and are subject to certain factors, risks and uncertainties that may cause actual results, outcome of events, timing and performance to differ
materially from those expressed or implied by such forward-looking statements. These risks include, but are not limited to, risks and uncertainties regarding the Company's ability to accurately estimate the actual research and development expenses and other costs associated with
the preclinical and clinical development of our product candidates, the adequacy of our capital resources and the availability of additional funding, risks and uncertainties regarding the Company's ability to successfully conduct preclinical and clinical studies of its product candidates, including those clinical trials noted in this press release,
risks and uncertainties that clinical trial results at any phase of
development may be adverse or may not be predictive of future result or lead to regulatory approval of any of the Company's product candidates, and risks and uncertainties relating to regulatory oversight, intellectual property claims, the timing, scope, cost and outcome of legal proceedings, future capital needs, key employees, dependence on the Company's collaborators and manufacturers, markets, economic
conditions, products, services, prices, reimbursement rates, competition and other risks detailed in the Company's public filings with the Securities and Exchange Commission, including ARIAD's Annual Report on Form 10-K for the fiscal year ended December 31, 2003. The information contained in this document is believed to be current as of the date of original issue. The Company does not intend to update any of the
forward-looking statements after the date of this document to conform these statements to actual results or to changes in the Company's expectations, except as required by law.
###
CONTACT: Tom Pearson
(610) 407-9260
Kelly Lindenboom
(617) 621-2345

HUMAN GENOME SCIENCES REPORTS RESULTS OF ONGOING PHASE 1 CLINICAL TRIALS OF HGS-ETR1 IN PATIENTS WITH ADVANCED CANCERS

- Results of Phase 1 clinical studies support further evaluation of HGS-ETR1 in Phase 2 clinical trials both as a single agent and in combination with chemotherapy -

- Data presented at 16 th EORTC-NCI-AACR Symposium on Molecular Targets and Cancer Therapeutics -

ROCKVILLE, Maryland – September 29, 2004 – Human Genome Sciences, Inc. (Nasdaq: HGSI) announced today that the results of ongoing Phase 1 clinical trials demonstrate the safety and tolerability of HGS-ETR1 (agonistic human monoclonal antibody to TRAIL Receptor 1) 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.

Safety, pharmacokinetic and biological activity data from two Phase 1 studies of HGS-ETR1 were presented today at the 16^th EORTC-NCI-AACR Symposium on Molecular Targets and Cancer Therapeutics in Geneva, Switzerland. The conference is jointly organized by the European Organisation for Research and Treatment of Cancer (EORTC), National Cancer Institute (NCI) and American Association for Cancer Research (AACR).

In an oral presentation at the EORTC-NCI-AACR Symposium’s plenary session, entitled “A Phase 1 Clinical Trial of HGS-ETR1, an Agonistic Monoclonal Antibody to TRAIL-R1, in Patients with Advanced Solid Tumors,” data were presented on thirty-nine patients treated to date in an ongoing open-label, dose-escalation clinical trial.¹ The median number of chemotherapeutic treatment regimens previously received was two, and ranged as high as nine. The patients were enrolled into seven cohorts (0.01, 0.03, 0.1, 0.3, 1.0, 3.0, or 10.0 mg/kg) and received HGS-ETR1 administered intravenously on a 28-day or 14-day schedule. The primary purpose of the study is to determine the safety, maximum tolerated dose (MTD), dose-limiting toxicities, and pharmacokinetics of HGS-ETR1 in patients with relapsed or refractory advanced tumors. Disease response also is being evaluated. Available tumor tissue samples from patients participating in the trial will be evaluated for expression of the TRAIL Receptor-1 protein using immunohistochemical (IHC) techniques.

Results to date of the ongoing Phase 1 clinical trial 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. No evidence of drug-related hematologic or hepatic toxicity has been observed at doses up to and including 10 mg/kg. The MTD has not been reached, and accrual in the trial continues at a dose of 10 mg/kg every 14 days. Dose-proportional pharmacokinetics were observed up to a dose of 1.0 mg/kg, with a terminal elimination half-life of 15 days. In seven patients treated at the 10 mg/kg dose level, the terminal elimination half-life of HGS-ETR1 was longer, averaging about 18 days. Some preliminary evidence of biological activity has been observed. Durable stable disease for greater than eight months was observed in one patient with metastatic sarcoma. Durable stable disease was observed for four months in one patient with head-and-neck cancer and in one patient with Ewing’s sarcoma; both patients continue on treatment.

A poster entitled “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” (Abstract #208) presented data on twenty-four patients treated to date in an open-label, dose-escalation clinical trial currently ongoing at two centers in Canada.² All patients admitted to the trial have relapsed or refractory disease and had received prior anti-cancer treatments (chemotherapy, radiotherapy, or hormone therapy). To date, twenty-four patients have been enrolled into five cohorts (0.01, 0.03, 0.3, 3.0, or 10.0 mg/kg) and received HGS-ETR1 administered intravenously every 28 days. Patients continue to be enrolled into the 10 mg/kg dose cohort. The study design calls for enrollment of an additional cohort at a dose of 20 mg/kg. Patients are treated every 28 days in the absence of disease progression or dose-limiting toxicities. The primary objective of the trial is to evaluate the safety and tolerability of repeated doses of HGS-ETR1 administered intravenously in patients with advanced solid tumors or non-Hodgkin’s lymphoma. The secondary objectives are to evaluate the pharmacokinetics of repeated doses of HGS-ETR1 and to assess tumor response.

Results to date of the ongoing clinical trial demonstrate that HGS-ETR1 is well tolerated with no clearly attributable toxicities to date and that the MTD has not been reached. The median number of treatment cycles delivered is two (1-12). Stable disease has been observed in eight patients for greater than two cycles. Preliminary data indicate that the pharmacokinetics of HGS-ETR1 are dose-proportional up to 0.3 mg/kg. The trial continues to enroll patients.

An additional poster presented at the EORTC-NCI-AACR Symposium, “Variable Distribution of TRAIL Receptor 1 in Primary Human Tumor and Normal Tissues” (Abstract #225), described the results of a preclinical study designed to identify specific malignancies that are most likely to express TRAIL Receptor 1.³ Such malignancies could be strong candidate indications for HGS-ETR1. The study, conducted by scientists at Human Genome Sciences in collaboration with scientists from DakoCytomation ⁴ and Fox Chase Cancer Center, used a highly specific immunohistochemical assay to evaluate TRAIL-R1 in human tumor and normal tissue. Of the first 134 malignancies evaluated, a total of 87 tumors (65 percent) showed some degree of TRAIL-R1 specific staining. TRAIL-R1 specific staining was consistently weak or absent in all 17 normal tissues assayed. Tumors of the pancreas, colon and lung were the most likely to have substantial staining for TRAIL-R1. Prostatic carcinomas were least likely to demonstrate TRAIL-R1 staining. The level of TRAIL-R1 protein in the colon was explored further in 26 additional samples representative of typical neoplastic progression. TRAIL-R1 staining distribution and intensity were increased in malignancies of the colon as compared to benign lesions or focal carcinomas in situ.

Roger B. Cohen, M.D., Director, Phase 1 Clinical Trials Program, Fox Chase Cancer Center, Philadelphia, said, “The Phase 1 clinical results we presented today demonstrate that HGS-ETR1 is well tolerated and can be safely and repetitively administered to patients with advanced malignancies. We have seen no evidence of drug-related hematological or hepatic toxicity at the dose levels administered to date. We have not reached a maximum tolerated dose, and we have seen preliminary evidence of biological activity. Patient accrual continues in the ongoing Phase 1 trials. Further evaluation of HGS-ETR1 is appropriate in Phase 2 clinical trials, both as a single agent and in combination with chemotherapy.”

David C. Stump, M.D., Executive Vice President, Drug Development, said, “We continue to be encouraged by the results emerging from our ongoing Phase 1 clinical trials of HGS-ETR1. The data show that HGS-ETR1 is well tolerated in patients with advanced solid tumors or non-Hodgkin’s lymphoma. Stable disease has been observed in a number of patients in these studies as well. Based on the encouraging interim clinical results from our Phase 1 studies, along with the strongly supportive preclinical evidence^{1-3, 6-11}, we announced at the beginning of September that we have advanced HGS-ETR1 to a Phase 2 clinical trial in patients with relapsed or refractory non-small cell lung cancer.⁵ We plan to initiate additional Phase 2 clinical trials of HGS-ETR1 in the weeks and months to come.”

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.¹² 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.

For more information about HGS-ETR1, see www.hgsi.com/products/ETR1.html. Health professionals interested in more information about trials 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 (240) 314-4400, 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.

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Footnotes:

1. R.B. Cohen, et al. “A Phase 1 Clinical Trial of HGS-ETR1, an Agonistic Monoclonal Antibody to TRAIL-R1, in Patients with Advanced Solid Tumors.” 16th EORTC-NCI-AACR Symposium on Molecular Targets and Cancer Therapeutics, 2004: Oral Presentation.
2. S.J. Hotte, 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). 16th EORTC-NCI-AACR Symposium on Molecular Targets and Cancer Therapeutics, 2004: Abstract #208.
3. W. Halpern, et al. Variable Distribution of TRAIL Receptor 1 in Primary Human Tumor and Normal Tissues. 16th EORTC-NCI-AACR Symposium on Molecular Targets and Cancer Therapeutics, 2004: Abstract #225.
4. (HGSI Press Release) Human Genome Sciences Announces License Agreement with DakoCytomation for Development of Pharmacogenomic Diagnostic Assays. March 31, 2004.
5. (HGSI Press Release) Human Genome Sciences Advances Anti-Cancer Drug to Phase 2 Clinical Development. September 8, 2004.
6. A.W. Tolcher, 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.
7. L.H. Le, 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.
8. G.V. Georgakis, 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.
9. 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.
10. 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.
11. Ashkenazi A. et al. Safety and anti-tumor activity of recombinant soluble APO2 ligand. J Clin Inv July 1999; 104(2): 155-162.
12. (HGSI Press Release) Cambridge Antibody Technology and Human Genome Sciences Announce Second Drug Partnership. January 8, 2002.

FOR IMMEDIATE RELEASE
CONTACTS:
David C. Stump, M.D.
Executive Vice President, Drug Development
240/314-4400
Jerry Parrott
Vice President, Corporate Communications
301/315-2777
Kate de Santis
Director, Investor Relations
301/251-6003

ARIAD REPORTS TUMOR REGRESSION WITH AP23573 AS A SINGLE AGENT
IN PATIENTS WITH RELAPSED AND/OR REFRACTORY CANCER

Updated Phase 1 Clinical Results on Novel mTOR Inhibitor Presented at
International Cancer Symposium

Cambridge, MA, September 30, 2004 – ARIAD Pharmaceuticals, Inc. (Nasdaq:
ARIA) today
announced, for the first time, updated results of two Phase 1 clinical
trials of its novel mTOR
inhibitor, AP23573 as a single agent, showing documented tumor
regression in patients with
advanced cancers – most of whom had progressive disease upon entering
the trial and
virtually all of whom had failed alternative treatments. These clinical
results are being
presented today at the 2004 EORTC-NCI-AACR Symposium on Molecular
Targets and
Cancer Therapeutics in Geneva, Switzerland.
Combined Trial Results: Anti-tumor Responses
Of 49 evaluable patients in the two trials, tumor regression was
demonstrated in 9 patients (4
“partial responses” by RECIST with at least 30% reduction in tumor size
and 5 “minor
responses” with 15% to 29% reduction). In an additional 15 patients,
disease stabilization
was achieved. Overall, 49% (24 of 49) of the patients in the two trials
had documented antitumor
responses (including partial and minor responses and stable disease),
with a median
response of 5 months in those demonstrating anti-tumor responses,
extending to greater than
18 months – the longest treatment to date.
Anti-tumor responses were demonstrated in 9 different refractory and/or
relapsed cancers,
including all evaluable patients with sarcoma (5 of 5), kidney cancer (7
of 7) and lymphoma (1
of 1), as well as 2 of 3 patients with non-small cell lung (NSCL) cancer.
“We are extremely encouraged by the number of patients with relapsed
and/or refractory
cancer who demonstrated tumor regression with AP23573 in Phase 1
clinical trials, as well as
the breadth of tumors that are responding to our novel mTOR inhibitor,”
said Harvey J. Berger,
M.D., chairman and chief executive officer of ARIAD. “As a clinician, I
was particularly
struck by the results in one patient with a Ewing’s sarcoma who had
received nine prior
anticancer regimens. After four cycles of AP23573, CT scans showed a 62%
reduction in the
size of the mass; this patient continues on study. Phase 2 studies of
AP23573 are ongoing in
patients with hematologic cancers and solid tumors.”
Daily Dosing Trial Results
In the 27 evaluable patients in the daily dosing trial – the dosing
regimen being used in
current Phase 2 clinical trials – AP23573 produced tumor regression in 7
patients:

• Partial response – Sarcoma, lymphoma, and NSCL cancer (1 each)
• Minor response – Sarcoma, NSCL, kidney, and thyroid cancers (1 each).
An additional 9 patients in this trial had stabilization of their
disease (overall 59% with
anti-tumor response).
Weekly Dosing Trial Results
In the 22 evaluable patients in the weekly dosing trial, AP23573 also
produced tumor
regression in 2 patients, both with particularly difficult-to-treat
cancers, even when the drug
was administered only once each week:
• Partial response – Bladder cancer (1) (unconfirmed, repeat scans pending)
• Minor response – Mesothelioma, a form of chest-cavity cancer (1).
An additional 6 patients in this trial had stabilization of their
disease (overall 36% with antitumor
response).
Additional Combined Trial Results
The daily dosing trial is ongoing at the Institute for Drug Development,
Cancer Therapy and
Research Center, San Antonio (M. Mita, M.D. and A. Tolcher, M.D.), and
the weekly dosing
trial is ongoing at the University of Chicago Cancer Center (A. Desai,
M.D. and M. Ratain,
M.D.).
AP23573 has been well tolerated by patients in both trials, with
generally mild or moderate,
readily reversible adverse events. The dose-limiting toxicity was severe
oral mucositis, an
inflammatory irritation of the mucous membranes of the mouth and a
common finding in
cancer patients on various types of treatments.
Pharmacodynamic assays on patient samples demonstrated a good
correlation of blood levels
of AP23573 with inhibition of AP23573’s molecular target, the protein
mTOR. Greater than
90% inhibition was observed within 1 hour after dosing in all patients
in both trials. With
daily dosing of AP23573, there was sustained inhibition of mTOR activity
for up to 10 days in
the majority of patients studied.
The pharmacokinetic (blood-clearance) profile of AP23573 was found to be
highly predictable
and reproducible, with a median half-life of 49 hours for all patients
with complete data in the
two trials. In contrast to other mTOR inhibitors in clinical trials,
AP23573 was stable in vivo
and is not a pro-drug.
About AP23573
The small-molecule drug, AP23573, starves cancer cells and shrinks
tumors by inhibiting the
critical cell-signaling protein, mTOR, which regulates the response of
tumor cells to nutrients
and growth factors, and controls tumor blood supply and angiogenesis
through effects on
Vascular Endothelial Growth Factor (VEGF).
About the Company
ARIAD is engaged in the discovery and development of breakthrough
medicines to treat cancer
by regulating cell signaling with small molecules. The Company is
developing a comprehensive
approach to patients with cancer that addresses the greatest medical
need – aggressive and
advanced-stage cancers for which current treatments are inadequate.
ARIAD also has an
exclusive license to pioneering technology and patents related to
certain NF-κB treatment
methods, and the discovery and development of drugs to regulate NF-κB
cell-signaling activity,
which may be useful in treating certain diseases. Additional information
about ARIAD can be
found on the web at http://www.ariad.com.
Some of the matters discussed herein are “forward-looking statements”
within the meaning of the
Private Securities Litigation Reform Act of 1995. Such statements are
identified by the use of words
such as “anticipate,” “estimate,” “expect,” “project,” “intend,” “plan,”
“believe,” and other words and
terms of similar meaning in connection with any discussion of future
operating or financial
performance. Such statements are based on management’s current
expectations and are subject to certain
factors, risks and uncertainties that may cause actual results, outcome
of events, timing and
performance to differ materially from those expressed or implied by such
forward-looking statements.
These risks include, but are not limited to, risks and uncertainties
regarding the Company’s ability to
accurately estimate the actual research and development expenses and
other costs associated with the
preclinical and clinical development of our product candidates, the
adequacy of our capital resources
and the availability of additional funding, risks and uncertainties
regarding the Company’s ability
to successfully conduct preclinical and clinical studies of its product
candidates, risks and uncertainties
that clinical trial results, such as those noted in this press release,
at any phase of development may
be adverse or may not be predictive of future result or lead to
regulatory approval of any of the
Company’s product candidates, and risks and uncertainties relating to
regulatory oversight,
intellectual property claims, the timing, scope, cost and outcome of
legal proceedings, future capital
needs, key employees, dependence on the Company’s collaborators and
manufacturers, markets,
economic conditions, products, services, prices, reimbursement rates,
competition and other risks
detailed in the Company’s public filings with the Securities and
Exchange Commission, including
ARIAD’s Annual Report on Form 10-K for the fiscal year ended December
31, 2003. The information
contained in this document is believed to be current as of the date of
original issue. The Company does
not intend to update any of the forward-looking statements after the
date of this document to conform
these statements to actual results or to changes in the Company’s
expectations, except as required by
law.
###

CONTACT: Tom Pearson
(610) 407-9260
Kelly Lindenboom
(617) 621-2345