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   Parkinson's disease (PD) is a degenerative disease of the central nervous system that often impairs motor skills, speech, and other functions. Symptoms of the disease include resting tremor, bradykinesia and rigidity. The primary symptoms are the result of decreased stimulation of the motor cortex by the basal ganglia, normally caused by the insufficient formation and action of dopamine, which is produced in the dopaminergic neurons of the brain. Symptoms of the disease appear once 50-80% of dopamine neurons have died. Parkinson's disease is both chronic and progressive.


    Pathogenesis of Parkinson's Disease

    The mechanism by which neurons are lost in PD may be a results of the formation of Lewy bodies. Lewy bodies are the histological hallmark of PD. They are composed primarily of fibrillar α-synuclein-ubiquitin complexes that can not be directed to the proteasome for degradation. These complexes aggregate in neurons, forming Lewy bodies. Early in the disease, Lewy bodies appear in the olfactory bulb and lower brain stem. As PD progresses and becomes symptomatic, Lewy body deposition and dopaminergic cell loss occurs in the substantia nigra pars compacta (SNpc). The precise pathogenic pathway in which Lewy bodies cause cell death is not known. A common theory is that Lewy bodies cause oxidative stress, mitochondrial dysfunction, excitoxicity and inflammation. This leads to proteasomal dysfunction and improper protein metabolism, which promotes Lewy body formation. Neuronal dysfunctional and apoptosis follows in the progressive neurodegenerative process of PD.

    The locus ceruleus and substantia innominata are also involved in the degenerative process. Advanced PD exhibits prominent non-dopaminergic features and the serotonergic, noradrenergic, cholinergic and GABAergic pathways are compromised. Neurons are lost in the cortex, subcortex, brainstem and other peripheral autonomic sites. It is the loss of these non-dopaminergic pathways that is the major cause of the non-motor symptoms of PD, including cognitive decline and autonomic dysfunction.

     Recently, the role of mitochondria in PD pathogenesis has become apparent. In the substantia nigra of PD brains the activity of mitochondrial complex I is significantly reduced. Function is not reduced within other PD brain areas. Furthermore, all environmental toxins identified so far that cause parkinsonism are mitochondrial inhibitors of complex I.

     Both genetic and environmental factors are involved in the pathogenesis of PD, with a small percentage of cases known to be hereditary. Environmental factors that increase the risk of PD include living in a rural environment and increased exposure to herbicides and insecticides. Smoking and coffee consumption are known to reduce the risk of developing PD. α-Synuclein gene mutation or multiplication can cause autosomal-dominant PD; mutations in the gene encoding LRRK2 have also been linked to late-onset and famililal Parkinson's disease. Both genetic and environmental etiologies share a common pathogenic pathway.

    Pharmacological Intervention

    The main motor features that are characteristic of PD are mainly due to the loss of the nigrostriatal dopaminergic pathway. Pharmacological treatments of PD aim to improve symptoms by increasing dopaminergic stimulation or inhibiting cholinergic and/or glutamatergic stimulation. There are several ways to increase dopamine stimulation:

  ~Levodopa, a brain penetrant dopamine precursor, is metabolized to dopamine by dopa decarboxylase within the CNS.

  ~Dopamine D1, D2 and D3 receptor agonists can penetrate the blood-brain barrier (BBB) and activate pre- and post-synaptic dopamine receptors.

  ~Monoamine oxidase B (MAO-B) inhibitors prevent the metabolism of dopamine and hence increase the synaptic half-life of dopamine and the amount of dopamine taken back up into the presynaptic terminal.

  ~Catechol O-methyltransferase (COMT) inhibitors prevent the metabolism of levodopa to 3-O-methydopa.

     The improved understanding of the etiology and pathogenesis of PD has enabled a range of compounds to be tested as putative drugs for neuroprotection. These target a number of different points in the cascade that cause dopaminergic cell dysfunction and death, and several have shown efficacy in vitro and in vivo. The implication is that those which are effective in slowing progression of dopamine cell death by interfering with biochemical pathways of damage will also be effective in slowing non-dopaminergic cell damage.

Cat. No. Product Name CAS No. Information



A potent and selective inhibitor of both wild-type and G2019S mutant LRRK2 with IC50 of 6.6 and 2.2 nM, respectively; also inhibits LRRK2 A2016T with IC50 of 47.7 nM; substantially inhibits Ser910 and Ser935 phosphorylation of both wild-type LRRK2 and G2019S mutant at 0.1-0.3 uM in a variety of cell types; inhibits Ser935 phosphorylation in mouse brain; orally active.




Nebicapone (BIA 3-202, BIA3-202) is a potent, long-acting, reversible and competitive peripheral inhibitor of catechol-O-methyltransferase (COMT) with IC50 of 3.7 nM for rat brain COMT, much less potent for liver COMT with IC50 of 696 nM; enhances the availability of L-DOPA to the brain and reduces its O-methylation, Nebicapone (BIA 3-202, BIA3-202) is an adjunct to levodopa/carbidopa or levodopa/benserazide in the treatment of Parkinson's disease.


SUVN-G3031 dihydrochloride


SUVN-G3031 (SUVN-G 3031) is a potent, selective, orally active histamine H3 receptor (H3R) inverse agonist with Ki of 8.73 nM (hH3R); exhibited an IC50 of 20 nM with progressive inhibition of (R)-α-methylhistamine (0.03 µM) induced agonist activity in [35S]-GTPγS binding assay using CHO-K1 cells expressing human H3R membranes; reverses (R)-α-methylhistamine induced dipsogenia in vivo.




SUVN-G3031 (SUVN-G 3031) is a potent, selective, orally active histamine H3 receptor (H3R) inverse agonist with Ki of 8.73 nM (hH3R); exhibited an IC50 of 20 nM with progressive inhibition of (R)-α-methylhistamine (0.03 µM) induced agonist activity in [35S]-GTPγS binding assay using CHO-K1 cells expressing human H3R membranes; reverses (R)-α-methylhistamine induced dipsogenia in vivo.




A selective, potent and reversible nitrocatechol-type inhibitor of catechol-O-methyltransferase (COMT) for treatment of Parkinson's disease; also kills neuroblastoma (NB) cells in preclinical models by inhibition of COMT; induces oxidative stress leading to apoptosis and inhibition of tumor growth in Neuroblastoma; also is a potent Transthyretin (TTR) aggregation inhibitor.




A potent and NR2B-selective NMDA receptor antagonist; potently protects cultured hippocampal neurons from glutamate toxicity (IC50=10 nM); shows neuroprotective, analgesic, and anti-Parkinsonian effects in animal studies.


ITI214 free base


ITI-214 is a potent, selective phosphodiesterase 1 (PDE1) inhibitor with Ki of 58 pM, displays >1,000-fold selectivity over PDE4A/4D and other PDE isoforms; improves the memory processes of acquisition, consolidation, and retrieval across a broad dose range (0.1-10 mg/kg, po) without disrupting the antipsychotic-like activity of a clinical antipsychotic medication, shows potential for schizophrenia and Alzheimer's disease, movement disorders, attention deficit and hyperactivity disorders, and other central nervous system (CNS) and non-CNS disorders.


GNE-7915 tosylate


GNE-7915 tosylate (GNE7915 tosylate) is a highly potent, selective, and brain-penetrable LRRK2 inhibitor with IC50 of 1.9 nM; shows 1/187 kinases with 50% inhibition at 0.1 uM; possesses an ideal balance of LRRK2 cellular potency, broad kinase selectivity, metabolic stability, and brain penetration across multiple species.




AQW-051 is a novel, potent and selective, orally bioavailable, brain-penetrant α7 nAChR partial agonist with pKd of 7.56; displays high selectivity (>100-fold) over other nACh receptors; stimulates calcium influx in GH3–ha7-22 cells recombinantly expressing the human α7-nACh receptor with pEC50 of 7.41; facilitates learning/memory performance in mice; reduces l-Dopa-induced dyskinesias and extends the duration of l-Dopa effects in parkinsonian monkeys.




A novel 5-HT receptor antagonist for the treatment of Parkinson's disease.

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