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AtreMorine is a novel biopharmaceutical compound obtained through non-denaturing biotechnological procedures from the structural components of the Vicia faba L plant, for the prevention and treatment of Parkinson´s disease (PD) and related disorders.
E-PodoFavalin-15999 extract is the structural base of AtreMorine and a natural source of L-DOPA, with an average concentration of 25 mg per gram of AtreMorine; it also contains a plethora of other bioactive substances as vegetal proteins, unsaturated fatty acids, minerals and vitamins, vegetal fibre, starch, vegetal pigments (carotenes) and vegetal sterols (phytosterols).
The in vitro studies revealed that AtreMorine is a powerful neuroprotectant in:
(i) cell cultures of human neuroblastoma SH-SY5Y cells
(ii) hippocampal slices in conditions of oxygen and glucose deprivation
(iii) striatal slices under conditions of neurotoxicity induced by 6-OHDA
AtreMorine displayed neuroprotective and anti-inflammatory effects in different in vitro models, suggesting that this novel bioproduct can be of utility to protect neurons against neurodegenerative processes, especially dopaminergic neurons associated with PD pathogenesis.
The in vivo studies showed that AtreMorine:
(i) protects against 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine (MPTP)-induced dopaminergic neurodegeneration
(ii) inhibits MPTP-induced microglia activation and neurotoxicity in substantia nigra
(iii) improves motor function in mice with MPTP-induced neurodegeneration
The clinical studies showed that AtreMorine is a potent enhancer of dopaminergic neurotransmission, increasing plasma dopamine levels by 200- to 500-fold in patients with PD and related movement disorders. AtreMorine is effective in untreated patients who receive AtreMorine for the first time (never treated before with antiparkinsonian drugs) and in patients chronically treated with L-DOPA or other antiparkinsonian drugs.
AtreMorine is an optimal option to reduce and minimize the potential side effects of conventional antiparkinsonian drugs, as the “wearing-off” phenomenon, motor fluctuations and dyskinesia, systemic complications (gastrointestinal disorders, cardiovascular problems, hormonal dysregulation), and neuropsychiatric disorders (depression, anxiety, toxic psychosis).
The coadministration of AtreMorine with other antiparkinsonian drugs allows a dose reduction of conventional drugs by 25%–50%, with the enhancement of clinical benefits, reduction of short- and long-term adverse drug reactions and extending the therapeutic effect of conventional antiparkinsonian drugs.
AtreMorine induces an increase in plasma levels of noradrenaline and adrenaline in PD patients, with no changes in serotonin. This effect may explain, in part, its clinical and biochemical benefits. AtreMorine also induces a significant decrease in prolactin, GH and cortisol levels.
The prolactin and GH response to AtreMorine can be directly attributed to the effect of L-DOPA on dopamine and noradrenaline synthesis and release, with the consequent increase in central and peripheral dopamine and noradrenaline levels. In contrast, the effect on cortisol might be primarily influenced by a direct effect of dopamine, noradrenaline, and adrenaline on the adrenal gland, and secondarily by the pituitary and / or hypothalamic regulation of ACTH, which in plasma did not show any significant changes.
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