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Allon Therapeutics AL-108 Human Efficacy Data Presented to Two ICAD 2008 Scientific Workshops

July 30, 2008

CHICAGO, ILLINOIS–(Marketwire – July 30, 2008) – Allon Therapeutics Inc. (TSX:NPC) –

Clinical trial data presented today to two scientific workshops at the International Conference on Alzheimer’s Disease and Related Disorders (ICAD 2008) validate the therapeutic potential of addressing the “tangles” component of the classic Alzheimer’s “plaques and tangles” pathology.

The data from a clinical trial evaluating drug candidate AL-108 in 144 patients with amnestic mild cognitive impairment (aMCI), a precursor to Alzheimer’s disease, demonstrated that specific memory function improved in patients who were given AL-108 over 12 weeks.

The clinical data was presented in an oral session by Professor Illana Gozes of Tel Aviv University, discoverer of AL-108 and Chief Scientific Officer of Allon Therapeutics Inc., and in a poster session by Dr. Donald E. Schmechel, a Duke University geriatrics professor, who was the principal investigator of the clinical trial. Prof. Gozes presented to a workshop reviewing alternative Alzheimer’s therapies and Dr. Schmechel’s poster was selected for ICAD’s Hot Topics session.

Prof. Gozes and Dr. Schmechel said the clinical trial data support the results of several studies in animals that show AL-108 reduced the classic Alzheimer’s “tangles” pathology and also increased memory function.

Dr. Schmechel’s presentation said the trial in aMCI patients demonstrated statistically significant, dose-dependent and durable improvements on key endpoints that measure short-term recall and working memory – two types of memory that are clinically relevant in Alzheimer’s disease. In this trial AL-108 was safe and well tolerated by patients. The most commonly reported side effects in subjects treated with AL-108 were headache and nasal congestion or irritation.

“Successfully impacting these specific memory domains indicates AL-108 is active in the regions of the brain responsible for their function – primarily the medial temporal lobe, hippocampus and prefrontal cortex,” Dr. Schmechel said.

“This positive aMCI clinical trial data makes AL-108 the first drug to validate in humans the potential of the ‘tangle’ pathway in memory disorders present in Alzheimer’s disease.”

AL-108 is being developed by Allon Therapeutics (TSX:NPC), a Canadian biotechnology company located in Vancouver. The drug was discovered by Prof. Gozes of the Sackler Faculty of Medicine at Tel Aviv University. Collaborative research led by Prof. Gozes has been supported by Tel Aviv University and the U.S. National Institutes of Health.

Supporting animal data:

AL-108 halts and reserves ‘tangles’

Animal data presented today at ICAD by Prof. Gozes and Dr. Matsuoka demonstrate that AL-108 halts and reverses the formation of “tangles”. AL-108 is derived from an eight amino acid peptide (NAPVSIPQ: “NAP”) synthesized from a naturally occurring neuroprotective brain protein known as activity dependent neuroprotective protein (ADNP).

Neurofibrillary tangles are the result of degeneration of microtubules, key components of the communication and transport pathways inside brain cells. Tangles occur when tau protein, which normally acts to hold microtubules together, converts from a soluble to an insoluble form, a process known as hyperphosphorylation.

During her oral presentation, Prof. Gozes told the ICAD session that the latest animal studies show that treatment with AL-108 reverses the degeneration of microtubules and increases their density by increasing the levels of soluble tau.

“These results suggest molecular and cellular specificity for NAP effects on microtubules. NAP interaction with microtubules is translated in vivo to decreased tau pathology, increased neuroprotection and enhanced cognitive function,” said Prof. Gozes.

Dr. Matsuoka’s poster presentation reported on a study he conducted on triple transgenic mice, bred to develop beta-amyloid plaques and neurofibrillary tangles and to exhibit behavioural deficits associated with AD.

Dr. Matsuoka’s study demonstrated that AL-108 treatment of triple transgenic mice causes a significant improvement in the performance of tasks involving spatial learning and memory as well as a statistically significant 70% decrease in the level of tau phosphorylation and a 20% reduction in beta amyloid plaques.

About the aMCI human trial

The Phase IIa trial was a double-blind, randomized, placebo- controlled, multiple-dose study to evaluate the safety, tolerability and effect on cognitive function of AL-108 after 12 weeks of intranasal administration in patients with aMCI. Clinically, patients with aMCI demonstrate memory impairment with otherwise normal cognition.

Several aspects of cognitive function were evaluated. The trial was conducted at 17 sites in the United States in 144 patients aged 55 to 85 years and evenly divided between genders.

Trial results

Cognitive function was measured in the aMCI patients by tests that are widely-used and validated in clinical trials evaluating patients with mild cognitive impairment and Alzheimer’s disease.

Prior to receiving drug or placebo, the cognitive function of each patient was measured with these tests. These results became the baseline for each patient’s performance during the trial.

Patients were treated for 12 weeks and tested at weeks four, eight, 12 and 16. Each patient’s test results were compared with his or her baseline performance and to other treatment groups.

A significant, dose-dependent and durable improvement was seen in two tests that measure short-term recall and working memory – delayed-match-to-sample and digit span. The high dose (15 mg twice daily) group showed a 62.4% improvement from baseline (p equals 0.038, versus placebo) in the delayed-match-to-sample 12-second delay test by the end of the trial. Similarly, the high dose group showed a 17.2% increase from baseline (p equals 0.028, versus placebo) in the digit span forward test.

The primary end-point for the trial was a composite of several cognitive tests (composite cognitive memory score, or CCMS) that measured memory and executive function. Patients treated with AL- 108 showed statistically significant improvement on tests that measured short-term recall and working memory, but no improvement on tests that involved executive functions, such as planning, cognitive flexibility and abstract thinking.

This divergence in results explains why the composite primary endpoint was trending toward, but did not achieve, statistical significance.

This data suggests that patients with aMCI have significant memory impairment but no significant impairment of executive function. Thus, AL-108 appears to have an impact on regions of the brain that are impaired in aMCI such as those that are known to control memory (medial temporal lobe, hippocampus and prefrontal cortex). However, no measurable effect of AL-108 on executive function was seen in this population since they were not impaired on tests that involve executive function such as Paired Associates Learning, Spatial Working Memory and One-Touch Stockings of Cambridge.

AL-108 was safe and well tolerated in this study. Overall, the incidence of adverse events between the placebo group and the AL- 108 group was similar with most adverse events being mild to moderate. Headache (13%), nasopharyngitis (8%), and nasal discomfort (4%) were the most common adverse events reported in subjects receiving AL-108 and were more frequent in subjects receiving AL- 108 than those receiving placebo.

The rates of discontinuations for adverse events were low and similar between the placebo and AL-108 groups.

About aMCI and Alzheimer’s Hallmarks

There is increasing evidence that some forms of cognitive impairment are precursors to Alzheimer’s disease. Amnestic mild cognitive impairment (aMCI) is a subset of MCI in which only the memory components of an individual’s function are affected.

Scientists agree that the brains of Alzheimer’s patients are characterized by two classic hallmarks of the disease: amyloid beta plaque accumulation outside neurons and neurofibrillary tangles inside neurons. No drug on the market today has any impact on these plaques and tangles.

Scientific studies have shown that the pathology of aMCI and Alzheimer’s is similar. For example, amyloid beta plaques and neurofibrillary tangles occur in both. Allon’s extensive animal data show that AL-108 dramatically reduces neurofibrillary tangles, reduces plaques, and that treated animals have significantly improved cognition. AL-108 is the first drug in development to have shown reduction of both neurofibrillary tangles and amyloid beta plaques in animals.

About ICAD 2008

The International Conference on Alzheimer’s Disease and Related Disorders (ICAD 2008) is being held in Chicago July 26-30. ICAD 2008 is organized by the Alzheimer’s Association, the leading U.S. voluntary health organization in Alzheimer’s care, support and research. The conference is bringing together more than 5,000 researchers, physicians and care providers from 60 countries – the largest group of international leaders in Alzheimer research and care ever convened.

About Allon’s neuroprotective platforms

Allon’s two neuroprotective technology platforms are based on two naturally occurring proteins secreted by the brain in response to a range of insults. The platforms are activity-dependent neuroprotective protein (ADNP) and activity-dependent neurotrophic factor (ADNF). Because the two platforms are based on different proteins, the drugs from each are different molecules with different therapeutic mechanisms and distinct commercial opportunities. Clinical-stage drugs AL-108 and AL-208 are derived from ADNP, while preclinical stage drug AL-309 is derived from ADNF.

About Allon

Allon Therapeutics Inc. is a clinical-stage biotechnology company developing treatments for major neurodegenerative conditions. In Q1 2008, Allon’s drug AL-108 demonstrated human efficacy in amnestic mild cognitive impairment, a precursor to Alzheimer’s disease. Allon has Phase II human efficacy programs pursuing three large underserved markets: Alzheimer’s disease, stroke and schizophrenia- related cognitive impairment. The Company is listed on the Toronto Stock Exchange under the trading symbol “NPC” (Neuro Protection Company(TM)) and based in Vancouver. For additional information please visit the Company’s website: www.allontherapeutics.com.

Forward Looking Statements

Statements contained herein, other than those which are strictly statements of historical fact may include forward-looking information. Such statements will typically contain words such as “believes”, “may”, “plans”, “will”, “estimate”, “continue”, “anticipates”, “intends”, “expects”, and similar expressions. While forward-looking statements represent management’s outlook based on assumptions that management believes are reasonable, forward- looking statements by their nature are subject to known and unknown risks, uncertainties and other factors that may cause the actual results, events or developments to be materially different from any future results, events or developments expressed or implied by them. Such factors include, among others, the inherent uncertainty involved in scientific research and drug development, Allon’s early stage of development, lack of product revenues, its additional capital requirements, the risks associated with successful completion of clinical trials and the long lead-times and high costs associated with obtaining regulatory approval to market any product which Allon may eventually develop. Other risk factors include the limited protections afforded by intellectual property rights, rapid technology and product obsolescence in a highly competitive environment and Allon’s dependence on collaborative partners and contract research organizations. These factors can be reviewed in Allon’s public filings at www.SEDAR.com and should be considered carefully. Readers are cautioned not to place undue reliance on such forward-looking statements and Allon disclaims any obligation to update or announce changes in any such factors except in its periodic filings.

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