A MEDICAMENT COMPRISING ANABASINE FOR TREATMENT OF ASTHMA, CHEST ALLERGY AND ATOPIC DERMATITS

Technical Field

Therapeutic drugs discovery .

Background Art

All approved drugs which medicate all asthmatics types or patients of chest allergy and atopic dermatitis are symptomatic types , non therapeutic .

Disclosure Of Invention

1- The innovative element in current medicament that, in contrast of related approved types, that it normalizes and treats all asthmatics types and patients of chest allergy and atopic dermatitis permanently and releases them from their chronic pathological phenomenons .

2- current medicament comprises of (L)(-)Anabasine as an active ingredient at 0.1 : 0.15 mg/kg of body weight and a pharmacologically acceptable excipient , diluent or carrier .

3- Medicament at mentioned doses is described to be administered by oral route twice per day for a period from 30 : 40 days for asthmatics and patients of chest allergy according to severity and condition development and from 21 : 40 days for patients of atopic dermatitis according to severity and condition development . Herein medication is one course only .

4 - As fundamental causes of asthma types , chest allergy and atopic dermatitis are not completely understood to date , administering current medicament as described terminates them permanently . In light of publications which are free from binding between anabasine and asthma or allergic diseases and also free from detecting efforts to develop anabasine as a human drug or trials to generate a hope for that , mentioned unique effect is probably elucidated as anabasine has a full agonist action on a7 nicotinic acetylcholine receptors which found in the central and peripheral nervous system, muscle, and many other tissues of human body. At the neuromuscular junction . So repeated ( L ) anabasine administering as described above to patients of same conditions at this minor concentration, for one course , so far from reported toxic dose and also teratogenic dose which was reported at 2.6 mg/kg animals body weight , this administering causes nicotinic acetylcholine receptors heterologous desensitization which may has the pivotal role in normalizing and treating them permanently via the mechanism of nicotinic acetylcholine receptors function modulation by phosphorylation beside the induced conformational changing in them particularly in alpha7 ligand binding domain . Receptors function modulation also may last longly after removal of (L) anabasine due to the permanent loss of functional channels within prolonged desensitizationfSimasko et al.,1986;Boyd,1987; Lukas, 1991; Buisson and Bertrand, 2002 ). This administering also negatively adapts signaling pathways . ALL these mutations may lead to a specific cholinergic modulation of allergic effector cells. mast cells, basophils, and eosinophils. Furthermore this desensitization also shapes cholinergic signaling which regulates and drives skeletal muscles contraction including airways smooth muscle, which plays an integral part in the pathophysiology of asthma. It is responsible for acute bronchoconstriction, which is potentiated by constrictor hyper responsiveness, impaired relaxation and length adaptation .Thus this shaping may modulate or normalize its contractile properties . On the other hand , nicotinic acetylcholine receptors in the peripheral nervous system transmit outgoing signals from the presynaptic to the postsynaptic cells within the sympathetic and parasympathetic nervous system , Heterologous desensitization also may thereafter leads these receptors to internalization . Role of receptor-mediated endocytosis is will recognized up take downregulation of transmembrane signal transduction but can also promote sustained signal transduction . It is actively implicated in transducing signals from the cell periphery to the nucleus . Herein noteworthy point , After receptors-mediated endocytosis process resulting it has been proposed that there are mechanismsrtpermanentlyf) downregulating incoming all antecedent signals are strong enough to shut down signaling completely without additional signal- transducing mechanisms .Considering that nAChRs are expressed in many regions of central and peripheral nervous system and a7nAChR is present in various non neuronal tissues as lung cells , epithelial cells , fibroblasts , endothelial cells , blood cells , gila and all types of immune cells , antecedent mechanisms which downregulate incoming signals permanently likely have an integral key role in terminating asthma types , chest allergy and atopic dermatitis permanently . These mechanisms sequently are attributed to nAChRs internalization induced by heterologous desensitization resulted in prolonged nAChRs exposure to low concentration of a 7nAChR agonist (L) anabsine . Chemical Structure DepictionAnabasine