AMGEN/GUILDFORD PHASE II RESULTS

[Perry Cohen <PerryC202@xxxxxxx>]

Guilford Pharmaceuticals Inc. (ticker: GLFD, exchange: NASDAQ) News Release - 
7/26/2001


--------------------------------------------------------------------------------
Guilford Pharmaceuticals Announces Completion Of NIL-A Phase II Clinical Trial 
for Parkinson's Disease

BALTIMORE, July 26 /PRNewswire/ -- Guilford Pharmaceuticals Inc. (Nasdaq: GLFD) 
announced today that Amgen Inc. has completed a Phase II clinical trial of 
NIL-A, the neuroimmunophilin ligand licensed to it by Guilford Pharmaceuticals, 
in patients with Parkinson's disease. This trial is the first clinical 
evaluation of a neuroimmunophilin ligand in the treatment of Parkinson's 
disease.

About the NIL-A Phase II Clinical Trial

The clinical trial conducted by Amgen is a Phase II, randomized, double- blind, 
placebo- controlled evaluation of the safety, pharmacokinetics and efficacy of 
NIL-A in patients with mild to moderate Parkinson's disease.

Phase II clinical trials of a drug are usually conducted to extend the safety 
evaluation conducted in Phase I, to determine a dosing regimen for future 
clinical trials, and to explore the potential efficacy of the drug in a 
targeted patient population. The efficacy evaluation centers on determining the 
clinical benefit of treatment, if any, and whether or not all patients or a 
subgroup appear to benefit. Phase II trials are usually exploratory or 
hypothesis generating. Confirmatory evidence, gathered in Phase III trials, is 
almost always needed before final conclusions can be drawn about the safety and 
efficacy of a new drug.

At the 42 participating medical centers in the NIL-A Phase II trial, patients 
were screened to determine their eligibility for the study and informed consent 
was obtained from each patient who was offered and accepted enrollment. 
Patients then received a thorough examination, including a neurological exam, 
to determine the extent and severity of their disease and all drugs then being 
administered were recorded. To be eligible, patients had to be optimally 
treated with antiparkinsonian drugs and have stable clinical symptoms. Upon 
completing the baseline evaluation, patients were randomly assigned to receive 
either placebo tablets, 200 mg of NIL-A, or 1,000 mg of NIL-A four times a day 
for 24 weeks. The randomization scheme was blocked by imaging status (see 
below) but not by treatment center.

Subsequently, all patients were periodically evaluated by neurologists expert 
in Parkinson's disease to determine if they had experienced any side effects 
from treatment, to measure their blood levels of NIL-A, and to determine if 
they had experienced any change in their symptoms of Parkinson's disease.

SPECT brain scans were obtained with 123I Beta-CIT (DOPASCAN(R) Injection) in a 
subset of the patients to obtain a measure of the density of dopamine nerve 
terminals in the region of the brain that deteriorates in Parkinson's disease.

After six months of treatment, final clinical examinations and SPECT scans were 
obtained and treatment was discontinued. Patients were followed for 28 days 
after treatment and then exited from the trial.

There were 300 patients enrolled in the trial, 101 were assigned to the placebo 
group, 100 to the low dose group, and 99 to the high dose group. SPECT scans 
were obtained in 105 subjects equally divided among the treatment groups.

The two primary clinical hypotheses tested in this trial were that 6 months of 
treatment with NIL-A would result in at least a 4 point improvement when 
compared with placebo in the UPDRS Motor Subscale measured before patients took 
their first daily dose of antiparkinsonian medication, and that NIL-A would be 
safe and well tolerated at doses up to 1000 mg four times a day for 6 months. 
The a priori efficacy hypothesis was established based on expert advice and 
prior experience with the development of other classes of antiparkinsonian 
drugs, although there was no prior clinical experience with NIL-A to generate 
the primary efficacy hypothesis. Secondary efficacy endpoints identified in the 
analytical plan for the trial were: 123I Beta CIT SPECT scans, total UPDRS 
score, bilateral finger tapping, dyskinesia rating scale, Hoehn & Yahr rating 
scale and a quality of life measure obtained from a questionnaire.

The frequency and severity of reported adverse events were similar in all three 
treatment groups except that patients in the high dose NIL-A group experienced 
an increased incidence of transient nausea or indigestion. The mean change in 
UPDRS motor score was -1.05 in placebo treated patients and 0.25 and -0.35 in 
the low dose and high dose patients respectively. (p=0.2) An increase in score 
indicates worsening disease. The mean percent change in the density of dopamine 
nerve terminals as measured by SPECT was +3.4% in placebo patients, +6.3% in 
low dose patients and +9.4% in the high dose group after 12 weeks of treatment. 
(n=30, 10 per group, p=0.4) the corresponding changes at 24 weeks were -0.15%, 
-1.2% and +2.5%. (n=105, 35 per group, p=0.7). The Hoehn & Yahr score improved 
(i.e., went down) during the trial in 11% of placebo patients, 17% of low dose 
patients, and 21% of the high dose patients. The difference between the high 
dose group and the placebo group was signific
 a!
nt after adjustment for age, dur
ation of Parkinson's disease symptoms, and Hoehn & Yahr score at baseline 
(p=0.028). The changes in the dyskinesia scores and finger tapping tests were 
not statistically significant.

Subgroups of patients stratified by age, disease severity, duration of 
symptoms, and type of antiparkinson's treatment are currently being analyzed.

These results suggest that NIL-A at doses up to 1000 mg taken orally four times 
a day for 6 months is well-tolerated but does not produce a substantial 
reversal of the motor symptoms of Parkinson's disease.

About Parkinson's Disease

Parkinson's disease is a chronic, progressive degenerative disorder that 
involves a specialized region of the brain that controls muscle tone and 
coordination. Most patients are affected in mid-life and usually develop hand 
tremors, muscle rigidity, and postural instability, among the many 
manifestations of the disease. The disease is caused by the degeneration of 
nerve cells that use dopamine as a chemical messenger. Treatment currently 
consists of administering drugs that increase the amount of dopamine in the 
affected regions of the brain or substitute for the lost dopamine. 
Unfortunately, there are no current treatments that can reverse, or even slow 
down, the progressive degeneration of the dopamine nerve cells in Parkinson's 
disease.

About Neuroimmunophilin Ligands

Neuroimmunophilin ligands are small molecules that in preclinical experiments 
have been shown to be orally-bioavailable, cross the blood-brain barrier, and 
repair and regenerate damaged nerves without affecting normal nerves. In 1997, 
Guilford entered into a collaboration with Amgen for the research, development 
and commercialization of a broad class of neuroimmunophilin ligands, for a 
range of indications, including Parkinson's disease, Alzheimer's disease, 
spinal cord injury, brain trauma, and other diseases and conditions. Amgen 
commenced the current Phase II trial for NIL-A for Parkinson's disease in the 
summer of 2000.

Guilford Pharmaceuticals is a biopharmaceutical company engaged in the 
development of polymer-based therapeutics for cancer, and novel products for 
the diagnosis and treatment of neurological diseases, including Parkinson's 
disease, Alzheimer's disease, stroke, severe head trauma, spinal cord injuries, 
multiple sclerosis and peripheral neuropathies.

Internet address: www.guilfordpharm.com

This press release contains forward-looking statements that involve risks and 
uncertainties, including those described in the section entitled "Risk Factors" 
contained in the Company's Registration Statement on Form S-3 dated June 21, 
2001, that could cause the Company's actual results and experience to differ 
materially from anticipated results and expectations expressed in these 
forward-looking statements. Among other things, there can be no assurance that 
NIL-A will be shown in clinical trials to be a safe and effective drug for the 
treatment of Parkinson's disease or other conditions.

SOURCE Guilford Pharmaceuticals Inc.

CONTACT: Stacey Jurchison, +1-410-631-5022, or Angie Rubin, +1-410-631-6449, 
both of Guilford Pharmaceuticals/

----------------------------------------------------------------------
To sign-off Parkinsn send a message to: mailto:listserv@xxxxxxxxxxxxxxxxxxxx
In the body of the message put: signoff parkinsn