The company has discovered several non-dopaminergic NCEs intended for the treatment of Parkinson's disease (PD) symptoms. The lead compound, Neu-120, has been developed as adjunct therapy to levodopa in patients with motor fluctuations and in patients who do not tolerate optimal doses of levodopa.

It is a highly potent and selective uncompetitive NMDA receptor modulator aimed at improving motor control and reducing levodopa-induced dyskinesia.

It also inhibits MAO-B and GSK-3B activities in vitro. It does not interact with other receptors, transporters or enzymes.

It is expected to help on one hand to alleviate the symptoms of parkinsonism, and at the same time reduce severity or abolish drug-induced extrapyramidal reactions including dyskinesia that are associated with such increase.

Neu-120 has been tested in several experimental models of PD, completed Phase I study, and is currently entering a Phase IIa phase.

Parkinson's disease is an age-related neurodegenerative disorder that affects approximately 1 percent of Americans over 50 years of age, but unrecognized early symptoms of the disease may be present in as many as 10 percent of those over 60 years of age.

The worldwide market for PD drugs was 1.6 million US$ in 1999. Clinically, the disease is characterized by a decrease in spontaneous movements (bradykinesia), gait difficulty, postural instability, rigidity, tremor and a variety of nonmotor symptoms. Levodopa-cabidopa combination (Sinemet) is the primary treatment for Parkinson's disease.

While Levodopa effectively alleviates all symptoms of Parkinson's disease and restores motor functions, within 3 to 5 years the majority of Parkinsonian patients develop levodopa-induced side-effects, mainly dyskinesias (involuntary and uncontrolled movements such as twisting and a hand or a limb) and wearing off (progressive shortening of theraputic response duration).

Dyskinesias are the most disabling side effects of long term levodopa therapy in Parkinsonian patients. There is currently no approved drug for levodopa-induced dyskinesia. The aetiology of levodopa-nduced dyskinesia is largely unknown.

There is now strong evidence that alterations in nondopaminergic neurotransmission systems within the basal ganglia may contribute to the appearance of motor response complications, particularly levodopa-induced dyskinesias. These alteration may include NMDA, adenosine A2A, adrenergic, 5-HT1A and 5HT2A, cannabinoid, and neuropeptide receptors. Amantadine (Symmetrel®) an NMDA receptor modulator, may help to smooth out fluctuations in performance and ameliorate levodopa induced dyskinesia. However, initial benefits may diminish with continued dosing.