CA2057456C - Anti depression pharmaceutical - Google Patents
Anti depression pharmaceuticalInfo
- Publication number
- CA2057456C CA2057456C CA002057456A CA2057456A CA2057456C CA 2057456 C CA2057456 C CA 2057456C CA 002057456 A CA002057456 A CA 002057456A CA 2057456 A CA2057456 A CA 2057456A CA 2057456 C CA2057456 C CA 2057456C
- Authority
- CA
- Canada
- Prior art keywords
- weeks
- adenine
- dinucleotide
- nicotinamide
- treatment
- Prior art date
- Legal status (The legal status is an assumption and is not a legal conclusion. Google has not performed a legal analysis and makes no representation as to the accuracy of the status listed.)
- Expired - Fee Related
Links
Classifications
-
- A—HUMAN NECESSITIES
- A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
- A61K—PREPARATIONS FOR MEDICAL, DENTAL OR TOILETRY PURPOSES
- A61K31/00—Medicinal preparations containing organic active ingredients
- A61K31/70—Carbohydrates; Sugars; Derivatives thereof
-
- A—HUMAN NECESSITIES
- A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
- A61P—SPECIFIC THERAPEUTIC ACTIVITY OF CHEMICAL COMPOUNDS OR MEDICINAL PREPARATIONS
- A61P25/00—Drugs for disorders of the nervous system
- A61P25/24—Antidepressants
-
- A—HUMAN NECESSITIES
- A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
- A61P—SPECIFIC THERAPEUTIC ACTIVITY OF CHEMICAL COMPOUNDS OR MEDICINAL PREPARATIONS
- A61P25/00—Drugs for disorders of the nervous system
- A61P25/26—Psychostimulants, e.g. nicotine, ***e
Landscapes
- Health & Medical Sciences (AREA)
- Life Sciences & Earth Sciences (AREA)
- Medicinal Chemistry (AREA)
- Veterinary Medicine (AREA)
- Public Health (AREA)
- General Health & Medical Sciences (AREA)
- Animal Behavior & Ethology (AREA)
- Pharmacology & Pharmacy (AREA)
- Chemical & Material Sciences (AREA)
- Neurology (AREA)
- Psychiatry (AREA)
- Chemical Kinetics & Catalysis (AREA)
- Nuclear Medicine, Radiotherapy & Molecular Imaging (AREA)
- Organic Chemistry (AREA)
- Neurosurgery (AREA)
- Biomedical Technology (AREA)
- Bioinformatics & Cheminformatics (AREA)
- Engineering & Computer Science (AREA)
- General Chemical & Material Sciences (AREA)
- Pain & Pain Management (AREA)
- Molecular Biology (AREA)
- Epidemiology (AREA)
- Pharmaceuticals Containing Other Organic And Inorganic Compounds (AREA)
- Saccharide Compounds (AREA)
- Compounds Of Unknown Constitution (AREA)
- Medicines Containing Material From Animals Or Micro-Organisms (AREA)
- Medicines Containing Plant Substances (AREA)
Abstract
Use of nicotinamide-adenine-dinucleotide, nicotinamide-adenine-dinucleotide phosphate or a physiologically compatible salt thereof for the treatment of depressions.
Description
_ ANTIDEPRESSANT
The invention relates to the novel use of nicotinamide-adenine-dinucleotide, nicotinamide-adenine-dinucleotide pho~phAte or a physiologically compatible salt thereof.
Depression is a neuroQsychiatric complaint, which influences the entirebehaviour, activity and emotional welfare of the person in question. It is known from a number of studies that ne~lol ~-Rm;tters, such as epinephrin (adrenaline), norepinephrin (noradrenaline), dopamine, serotonin or G~BA
( ~ -~m;nob~tyric aci~) play a part in the formation of depressive symptcms (p ~;~r~rer~ W. Birkmayer and E. Neumeyer, "The Tyrosin-Tryptophan-Diagram in a Longtime Study with Depressed Patientsn, Jcurnal of Neural Tr~nRm;~sion, 34, pp 31-48, 1973 (with the indication of further literature references)). Both biochemical analyses of the brains of dead depressive patients and blood and urine tests on precursors and metabolites of said ne~loLL~lsmitters in patients suffering frcm depression revealed that the ne~lo~ smitter equilibrium is disturbed in these patients.
Mcdern m~;c~mPntous treatment of depressive diseases is largely based on inhibiting the deccmposition of the ne~lu~L~lsmitters in the neurone, so as to enrich the stored neulu~l~lsmitters~ This is brought about by adminis-tering so-called MAO inhibitors, which block the e~7y--.e monoamine oxidase (MAO), which is largely responsible for the deccmposition of cate~h~l~m;nes and other substances in the neurone. However, although this treatment method is effective, it suffers frcm several seric~us disadvantages. Firstly the inhibiting of the deccmposition of n~u~ smitters present in the neurone only ;nfl~ nceR the overall concentration U,el~L, but has a lesser influence on the ~ ;hrium of the in~dividual neLluLl~lsmitters, so that e.g. it is not possible to compensate a deficit of a specific neurotrans-mitter as a result of functional ~;Ror~rs in production. The carrying out of therapy with M~O inhibitors must consequently take place in a very variable manner and must be specifically adjusted to each individual patient by a pssR;ble comh;n~tion with other ~e~;c~m~nts. Therefore such mr~ ents can only be ~m;n;Rtered under cont;~llols mF~;c~l control, because over~os~R can quickly occur and which then lead to lmple~R~nt side-effects, such as restl~sRness and insomnia. In addition, MAO inhibitor Ul~Lq~y constitutes a massive action in the neuronal functions of the 205~7456 _ - 2 -patient, whose effects have not yet been fully researched.
Therefore there was a need for a readily dosable antidepressant, which requires no constant m~;cal control or monitoring and which causes no side-effects.
It has surprisingly been found that the use of nicotinamide-adenine-dinucleotide, nicotinamide-adenine-dinucleotide ph~ph~te or a physiolog-ically compatible salt thereof is eminently suitable for the treatment of10 depressions.
It is known that nicotinamide-adenine-dinucleotide (NADH) can be success-fully used in the treatment of Parkinson's disease (EP 89 730 051.3).
Parkinson's disease is based on a disturbed dcpaminergic ne~loLl~l~nission in the basal ~gl;~ns~ generally due to an increasing decline of the ~op~m;nergic neurones initially in the substantia nigra, but during the disease also in other areas.
It has surprisingly been found in clinical research that the me~;~Am~nts proposed for the treatment of Parkinson's disease can be very successfully use in the treatment of depressions, in which the causes are of a very varied nature.
Preferably the nicot;n~m;~e~adenine-dinucleotide, the nicot;n~m;~e-adenine-dinucleotide L~h~slJh~te or the physiologically acc~able salt thereof is sl~pl;e~ to the bcdy in a quantity of 1 to S0 mg, preferably 5 to 12.5 mg as a single dose.
Further advantages and features of the invention can be y~Ule~d frcm the following des~Li~ion of cl;n;~l tests carried out in this connection.
A first series of tests c~rered 15 patients suffering frcn depressions having different origins. For assessing the disease use was ma~e of the so-called Bilhl~y~l depressian scale, which can be gathered fmm the bottam of table 1. The patients were tested before therapy and after a given treatment time.
Z(~57456 _ - 3 -The first group of patients consisted of 5 wanen and 10 men. The youngest patient was 26, the oldest 76. All patients received either parenterally or or~lly the reduced fonn of nicotinamide-adenine-dinucleotide (NADH).
The results are given in table 2. A second group of 15 patients, consisting of 8 wanen and 7 men (youngest patient 25, oldest 68) the reduced fonn of nicotinamide-adenine-dinucleotide phosphate (NADPH) was ~mini~tered~ once again either parenterally or or~lly. The results are given at the bottan of table 3.
m e therapy pericds lasted between 2 and 12 weeks. The individual appraisal on the basis of the Birhmayer scale before NADH or NADPH LLea~ t amcunted to 19 to 41 of a possible 80 points. Testing after therapy revealed a 63 to 97~ improvement campared with the values es~hl;~hf~ before therapy.
m ree (first grcup) or five (second group) of patients retu m ed to an a~nost completely norm~l behaviour with only one point in the 80 point scale, 0 point indicating an absolutely nonnal behaviour.
The results reveal that the treatment of depressions with NADH or NADPH
provided convincing improvements to the ~l;n;cAl picture after only a very short time.
In each case 6 patients in each group received the NADH or NADPH intraven-cusly, 2 intramuscularly and the rest orally. The dosage fluctuated between 1 and 50 mg, the best results being obtained when S to 12.5 mg were admin-istered. The intravenous A~m;n;~tration took place in the fonm of an infusion of 10 mg of NADH or NADPH in 200 ml of Elehest. Intravenous admin-istration took place three times weekly. Oral AAm;n;~tration took place daily or every other day. On the basis of the present results the nature of the ~m;n;~tration does not appear to have any significant influence on the improve~ent to the cl;n;~Al picture. No side-effects were observed (even after 12 weeks treatment).
The essential advantage of nicot;nAm;~e~ n;ne-dinucleotide and nicotin-amide-adenine-dinucleotide pho~phAte compared with the presently preferred antidepressants, i.e. MAO inhibitors, is the biological origin thereof.
Nicot;n~;~e-fl~n;ne-dinucleotide and nicot;n~m;~e-adenine-~;n~lrleot;~e 2Q5~456 _ - 4 -phosphate occurs in natural fonm in the human body and is the enzyme cofactor for a large number of dihydrogenases. The administration of nicot;n*mi~e-adenine-dinucleotide, nicot;n~m;~e-adenine-dinucleotide phos-phate or a physiologically compatible salt thereof does not directly affect the neural functions of the human being and instead aids in an as yet unexplained manner the making good of a disturbed neurotransmitter e~l;l;b-rium. A treatment with nicotinamide-adenine-dinucleotide, nicot;n~m;~e-adenine-~;nu~leotide ph~ph~te or a physiologically acceptable salt thereof can therefore be controlled without any problem and even without m~;c~l supervision cannot lead to owerdoses and therefore associated unpleasant side-effects, as are known in connection with MAO inhibitors.
The inventive features disclosed in the description and claims can be essential to the various embcdiments of the invention, either singly or in randam combination.
_ _ 5 _ Z Q 5 ~ 4 5 6 Depressian appraisal scale (Prof. W. Bilh-~yeL) Appraisal number Appraisal parameters 0 1 2 3 1. Listless 2. Gloomy 3. No interest 4. No drive 5. Lack of concentration 6. Reduced efficiency 7. Sleepless 8. No appetite 9. Weight decrease 10. Constipation 11. Loss of libido 12. Evening remission 13. Compulsive ~using 14. General pess~mism 15. Self-reproaches 16. Guilt feelings 17. Fear 18. ~l;r;~al t~n~ncy 19. Hypcchondriacal complaints 20. Thoughts concerning the pointlessness of life - 6 - 205~456 TABLE 2: NADH Therapy No. Sex Age Treatment Treatment Before After Improv~nents time 1 M 59 10 mg i.v. 5 weeks 29 1 96.5 3X weekly 2 M 53 6 mg i.m. 2 weeks 32 10 68.2 daily 3 M 26 6 mg i.v. 3 weeks 31 3 90.3 weekly 4 F 51 5 mg orally 5 weeks 41 5 87.8 3X weekly M 49 10 mg i.v. 4 weeks 26 1 96.2 3X weekly 6 M 71 10 mg orally 4 weeks 24 18 66.7 daily 7 M 76 6 mg i.v. 3 weeks 19 3 84.2 daily 8 M 49 10 mg i.v. 3 weeks 24 3 87.5 9 M 47 5 mg orally 12 weeks 31 11 64.5 daily F 69 12.5 mg i.v. 5 weeks 19 7 63.2 3X weekly 11 M 60 5 mg i.m. 28 1 96.5 3X weekly 12 F 36 5 mg orally 3 weeks 31 3 90.3 every other day 13 F 55 1 mg i.m. 6 weeks 35 4 88.6 3X weekly 14 F 29 50 mg or~lly 3 weeks 32 6 81.25 daily M 42 20 mg i.v. 10 weeks 28 9 67.9 3X weekly TABLE 3: NADPH THER~PY
No. Sex Age Treatment Treatment E~efore After ~r~prwenents time M 5110 mg i.v. 2 weeks 28 1 96.5 3X wee3cly 2 M 25 6 mg i.m. 3 weeks 19 6 68.4 daily 3 M 42 6 mg i.v. 5 weeks 24 5 79.2 weekly 4 F 37 5 mg orally 4 weeks 41 10 75.6 3X weekly F 60 10 mg i.v. 3 weeks 32 4 87.5 3X weekly 6 M 65 10 mg orally 2 weeks 28 3 89.3 daily 7 M 68 6 mg i.v. 3 weeks 35 1 97.1 daily 8 M 48 10 mg i.v. 4 wee~cs 32 11 65.6 da;ly 9 M 61 1 mg orally 5 weeks 28 3 89.3 da;lY
F 53 50 mg i.v. 2 weeks 31 1 96.8 3X weekly 11 F 60 5 mg i.m. 10 weeks 29 2 93.1 3X weekly 12 F 48 3 mg orally 4 weeks 20 1 95 every other day 13 F 53 7 mg i.m. 3 weeks 40 9 77.5 3X weelcly 14 F 27 15 mg i.v. 10 weeks 31 10 67.7 3X weekly F 67 50 mg orally 3 weeks 27 6 77.8 every other day
The invention relates to the novel use of nicotinamide-adenine-dinucleotide, nicotinamide-adenine-dinucleotide pho~phAte or a physiologically compatible salt thereof.
Depression is a neuroQsychiatric complaint, which influences the entirebehaviour, activity and emotional welfare of the person in question. It is known from a number of studies that ne~lol ~-Rm;tters, such as epinephrin (adrenaline), norepinephrin (noradrenaline), dopamine, serotonin or G~BA
( ~ -~m;nob~tyric aci~) play a part in the formation of depressive symptcms (p ~;~r~rer~ W. Birkmayer and E. Neumeyer, "The Tyrosin-Tryptophan-Diagram in a Longtime Study with Depressed Patientsn, Jcurnal of Neural Tr~nRm;~sion, 34, pp 31-48, 1973 (with the indication of further literature references)). Both biochemical analyses of the brains of dead depressive patients and blood and urine tests on precursors and metabolites of said ne~loLL~lsmitters in patients suffering frcm depression revealed that the ne~lo~ smitter equilibrium is disturbed in these patients.
Mcdern m~;c~mPntous treatment of depressive diseases is largely based on inhibiting the deccmposition of the ne~lu~L~lsmitters in the neurone, so as to enrich the stored neulu~l~lsmitters~ This is brought about by adminis-tering so-called MAO inhibitors, which block the e~7y--.e monoamine oxidase (MAO), which is largely responsible for the deccmposition of cate~h~l~m;nes and other substances in the neurone. However, although this treatment method is effective, it suffers frcm several seric~us disadvantages. Firstly the inhibiting of the deccmposition of n~u~ smitters present in the neurone only ;nfl~ nceR the overall concentration U,el~L, but has a lesser influence on the ~ ;hrium of the in~dividual neLluLl~lsmitters, so that e.g. it is not possible to compensate a deficit of a specific neurotrans-mitter as a result of functional ~;Ror~rs in production. The carrying out of therapy with M~O inhibitors must consequently take place in a very variable manner and must be specifically adjusted to each individual patient by a pssR;ble comh;n~tion with other ~e~;c~m~nts. Therefore such mr~ ents can only be ~m;n;Rtered under cont;~llols mF~;c~l control, because over~os~R can quickly occur and which then lead to lmple~R~nt side-effects, such as restl~sRness and insomnia. In addition, MAO inhibitor Ul~Lq~y constitutes a massive action in the neuronal functions of the 205~7456 _ - 2 -patient, whose effects have not yet been fully researched.
Therefore there was a need for a readily dosable antidepressant, which requires no constant m~;cal control or monitoring and which causes no side-effects.
It has surprisingly been found that the use of nicotinamide-adenine-dinucleotide, nicotinamide-adenine-dinucleotide ph~ph~te or a physiolog-ically compatible salt thereof is eminently suitable for the treatment of10 depressions.
It is known that nicotinamide-adenine-dinucleotide (NADH) can be success-fully used in the treatment of Parkinson's disease (EP 89 730 051.3).
Parkinson's disease is based on a disturbed dcpaminergic ne~loLl~l~nission in the basal ~gl;~ns~ generally due to an increasing decline of the ~op~m;nergic neurones initially in the substantia nigra, but during the disease also in other areas.
It has surprisingly been found in clinical research that the me~;~Am~nts proposed for the treatment of Parkinson's disease can be very successfully use in the treatment of depressions, in which the causes are of a very varied nature.
Preferably the nicot;n~m;~e~adenine-dinucleotide, the nicot;n~m;~e-adenine-dinucleotide L~h~slJh~te or the physiologically acc~able salt thereof is sl~pl;e~ to the bcdy in a quantity of 1 to S0 mg, preferably 5 to 12.5 mg as a single dose.
Further advantages and features of the invention can be y~Ule~d frcm the following des~Li~ion of cl;n;~l tests carried out in this connection.
A first series of tests c~rered 15 patients suffering frcn depressions having different origins. For assessing the disease use was ma~e of the so-called Bilhl~y~l depressian scale, which can be gathered fmm the bottam of table 1. The patients were tested before therapy and after a given treatment time.
Z(~57456 _ - 3 -The first group of patients consisted of 5 wanen and 10 men. The youngest patient was 26, the oldest 76. All patients received either parenterally or or~lly the reduced fonn of nicotinamide-adenine-dinucleotide (NADH).
The results are given in table 2. A second group of 15 patients, consisting of 8 wanen and 7 men (youngest patient 25, oldest 68) the reduced fonn of nicotinamide-adenine-dinucleotide phosphate (NADPH) was ~mini~tered~ once again either parenterally or or~lly. The results are given at the bottan of table 3.
m e therapy pericds lasted between 2 and 12 weeks. The individual appraisal on the basis of the Birhmayer scale before NADH or NADPH LLea~ t amcunted to 19 to 41 of a possible 80 points. Testing after therapy revealed a 63 to 97~ improvement campared with the values es~hl;~hf~ before therapy.
m ree (first grcup) or five (second group) of patients retu m ed to an a~nost completely norm~l behaviour with only one point in the 80 point scale, 0 point indicating an absolutely nonnal behaviour.
The results reveal that the treatment of depressions with NADH or NADPH
provided convincing improvements to the ~l;n;cAl picture after only a very short time.
In each case 6 patients in each group received the NADH or NADPH intraven-cusly, 2 intramuscularly and the rest orally. The dosage fluctuated between 1 and 50 mg, the best results being obtained when S to 12.5 mg were admin-istered. The intravenous A~m;n;~tration took place in the fonm of an infusion of 10 mg of NADH or NADPH in 200 ml of Elehest. Intravenous admin-istration took place three times weekly. Oral AAm;n;~tration took place daily or every other day. On the basis of the present results the nature of the ~m;n;~tration does not appear to have any significant influence on the improve~ent to the cl;n;~Al picture. No side-effects were observed (even after 12 weeks treatment).
The essential advantage of nicot;nAm;~e~ n;ne-dinucleotide and nicotin-amide-adenine-dinucleotide pho~phAte compared with the presently preferred antidepressants, i.e. MAO inhibitors, is the biological origin thereof.
Nicot;n~;~e-fl~n;ne-dinucleotide and nicot;n~m;~e-adenine-~;n~lrleot;~e 2Q5~456 _ - 4 -phosphate occurs in natural fonm in the human body and is the enzyme cofactor for a large number of dihydrogenases. The administration of nicot;n*mi~e-adenine-dinucleotide, nicot;n~m;~e-adenine-dinucleotide phos-phate or a physiologically compatible salt thereof does not directly affect the neural functions of the human being and instead aids in an as yet unexplained manner the making good of a disturbed neurotransmitter e~l;l;b-rium. A treatment with nicotinamide-adenine-dinucleotide, nicot;n~m;~e-adenine-~;nu~leotide ph~ph~te or a physiologically acceptable salt thereof can therefore be controlled without any problem and even without m~;c~l supervision cannot lead to owerdoses and therefore associated unpleasant side-effects, as are known in connection with MAO inhibitors.
The inventive features disclosed in the description and claims can be essential to the various embcdiments of the invention, either singly or in randam combination.
_ _ 5 _ Z Q 5 ~ 4 5 6 Depressian appraisal scale (Prof. W. Bilh-~yeL) Appraisal number Appraisal parameters 0 1 2 3 1. Listless 2. Gloomy 3. No interest 4. No drive 5. Lack of concentration 6. Reduced efficiency 7. Sleepless 8. No appetite 9. Weight decrease 10. Constipation 11. Loss of libido 12. Evening remission 13. Compulsive ~using 14. General pess~mism 15. Self-reproaches 16. Guilt feelings 17. Fear 18. ~l;r;~al t~n~ncy 19. Hypcchondriacal complaints 20. Thoughts concerning the pointlessness of life - 6 - 205~456 TABLE 2: NADH Therapy No. Sex Age Treatment Treatment Before After Improv~nents time 1 M 59 10 mg i.v. 5 weeks 29 1 96.5 3X weekly 2 M 53 6 mg i.m. 2 weeks 32 10 68.2 daily 3 M 26 6 mg i.v. 3 weeks 31 3 90.3 weekly 4 F 51 5 mg orally 5 weeks 41 5 87.8 3X weekly M 49 10 mg i.v. 4 weeks 26 1 96.2 3X weekly 6 M 71 10 mg orally 4 weeks 24 18 66.7 daily 7 M 76 6 mg i.v. 3 weeks 19 3 84.2 daily 8 M 49 10 mg i.v. 3 weeks 24 3 87.5 9 M 47 5 mg orally 12 weeks 31 11 64.5 daily F 69 12.5 mg i.v. 5 weeks 19 7 63.2 3X weekly 11 M 60 5 mg i.m. 28 1 96.5 3X weekly 12 F 36 5 mg orally 3 weeks 31 3 90.3 every other day 13 F 55 1 mg i.m. 6 weeks 35 4 88.6 3X weekly 14 F 29 50 mg or~lly 3 weeks 32 6 81.25 daily M 42 20 mg i.v. 10 weeks 28 9 67.9 3X weekly TABLE 3: NADPH THER~PY
No. Sex Age Treatment Treatment E~efore After ~r~prwenents time M 5110 mg i.v. 2 weeks 28 1 96.5 3X wee3cly 2 M 25 6 mg i.m. 3 weeks 19 6 68.4 daily 3 M 42 6 mg i.v. 5 weeks 24 5 79.2 weekly 4 F 37 5 mg orally 4 weeks 41 10 75.6 3X weekly F 60 10 mg i.v. 3 weeks 32 4 87.5 3X weekly 6 M 65 10 mg orally 2 weeks 28 3 89.3 daily 7 M 68 6 mg i.v. 3 weeks 35 1 97.1 daily 8 M 48 10 mg i.v. 4 wee~cs 32 11 65.6 da;ly 9 M 61 1 mg orally 5 weeks 28 3 89.3 da;lY
F 53 50 mg i.v. 2 weeks 31 1 96.8 3X weekly 11 F 60 5 mg i.m. 10 weeks 29 2 93.1 3X weekly 12 F 48 3 mg orally 4 weeks 20 1 95 every other day 13 F 53 7 mg i.m. 3 weeks 40 9 77.5 3X weelcly 14 F 27 15 mg i.v. 10 weeks 31 10 67.7 3X weekly F 67 50 mg orally 3 weeks 27 6 77.8 every other day
Claims (3)
1. Use of nicotinamide-adenine-dinucleotide (NADH), nicotinamide-adenine-dinucleotide phosphate (NADPH) or a physiologically compatible salt thereof for the treatment of depressions.
2. Use according to claim 1, characterized in that the nicotinamide-adenine dinucleotide (NADH), nicotinamide-adenine-dinucleotide phosphate (NADPH) or the physiologically compatible salt thereof is supplied to the body as a single dose in a quantity of 1 to 50 mg.
3. Use according to claim 2, characterized in that the single dose is 5 to 12,5 mg.
Applications Claiming Priority (2)
| Application Number | Priority Date | Filing Date | Title |
|---|---|---|---|
| DE4100361A DE4100361C1 (en) | 1991-01-04 | 1991-01-04 | |
| DEP4100361.6 | 1991-01-04 |
Publications (2)
| Publication Number | Publication Date |
|---|---|
| CA2057456A1 CA2057456A1 (en) | 1992-07-05 |
| CA2057456C true CA2057456C (en) | 1996-02-06 |
Family
ID=6422686
Family Applications (1)
| Application Number | Title | Priority Date | Filing Date |
|---|---|---|---|
| CA002057456A Expired - Fee Related CA2057456C (en) | 1991-01-04 | 1991-12-10 | Anti depression pharmaceutical |
Country Status (15)
| Country | Link |
|---|---|
| EP (1) | EP0493861B1 (en) |
| JP (1) | JP2519148B2 (en) |
| AT (1) | ATE148991T1 (en) |
| AU (1) | AU631755B2 (en) |
| BR (1) | BR9105183A (en) |
| CA (1) | CA2057456C (en) |
| DE (2) | DE4100361C1 (en) |
| DK (1) | DK0493861T3 (en) |
| ES (1) | ES2097181T3 (en) |
| GR (1) | GR3022724T3 (en) |
| HU (1) | HU213112B (en) |
| IE (1) | IE914477A1 (en) |
| NO (1) | NO179602C (en) |
| PT (1) | PT99962B (en) |
| ZA (1) | ZA9244B (en) |
Families Citing this family (4)
| Publication number | Priority date | Publication date | Assignee | Title |
|---|---|---|---|---|
| CA2167104A1 (en) * | 1995-01-17 | 1996-07-18 | Joerg G.D. Birkmayer | Nadh and nadph therapeutic agents for nasal, sublingual, rectal and dermal administration |
| US5712259A (en) * | 1996-04-22 | 1998-01-27 | Birkmayer Pharmaceuticals | NADH and NADPH pharmaceuticals for treating chronic fatigue syndrome |
| US5668114A (en) * | 1996-05-08 | 1997-09-16 | Birkmayer Pharmaceuticals | NADH and NADPH pharmaceuticals for treating hypertension |
| ES2953842A1 (en) * | 2023-07-17 | 2023-11-16 | Nuadi Europe S L | DUST HUBCAPS (Machine-translation by Google Translate, not legally binding) |
Family Cites Families (2)
| Publication number | Priority date | Publication date | Assignee | Title |
|---|---|---|---|---|
| US3341412A (en) * | 1966-03-04 | 1967-09-12 | Enzomedic Lab Inc | Methods of treating schizophrenia |
| US4970200A (en) * | 1988-03-01 | 1990-11-13 | Schering Aktiengesellschaft | Agent for treatment of Parkinson's disease |
-
1991
- 1991-01-04 DE DE4100361A patent/DE4100361C1/de not_active Expired - Lifetime
- 1991-11-07 DE DE59108553T patent/DE59108553D1/en not_active Expired - Fee Related
- 1991-11-07 DK DK91250304.2T patent/DK0493861T3/en active
- 1991-11-07 EP EP91250304A patent/EP0493861B1/en not_active Expired - Lifetime
- 1991-11-07 AT AT91250304T patent/ATE148991T1/en not_active IP Right Cessation
- 1991-11-07 ES ES91250304T patent/ES2097181T3/en not_active Expired - Lifetime
- 1991-11-28 BR BR919105183A patent/BR9105183A/en not_active Application Discontinuation
- 1991-12-10 CA CA002057456A patent/CA2057456C/en not_active Expired - Fee Related
- 1991-12-20 IE IE447791A patent/IE914477A1/en not_active IP Right Cessation
- 1991-12-27 JP JP3346474A patent/JP2519148B2/en not_active Expired - Fee Related
- 1991-12-31 AU AU90109/91A patent/AU631755B2/en not_active Ceased
-
1992
- 1992-01-02 PT PT99962A patent/PT99962B/en not_active IP Right Cessation
- 1992-01-03 ZA ZA9244A patent/ZA9244B/en unknown
- 1992-01-03 HU HU9200025A patent/HU213112B/en not_active IP Right Cessation
- 1992-01-03 NO NO920056A patent/NO179602C/en not_active IP Right Cessation
-
1997
- 1997-03-03 GR GR970400414T patent/GR3022724T3/en unknown
Also Published As
| Publication number | Publication date |
|---|---|
| HU213112B (en) | 1997-02-28 |
| HU9200025D0 (en) | 1992-03-30 |
| EP0493861A3 (en) | 1993-03-03 |
| DE59108553D1 (en) | 1997-03-27 |
| GR3022724T3 (en) | 1997-06-30 |
| ATE148991T1 (en) | 1997-03-15 |
| DE4100361C1 (en) | 1992-04-23 |
| NO179602C (en) | 1996-11-13 |
| PT99962A (en) | 1993-02-26 |
| JP2519148B2 (en) | 1996-07-31 |
| BR9105183A (en) | 1992-09-29 |
| EP0493861A2 (en) | 1992-07-08 |
| AU9010991A (en) | 1992-07-16 |
| EP0493861B1 (en) | 1997-02-19 |
| AU631755B2 (en) | 1992-12-03 |
| HUT60141A (en) | 1992-08-28 |
| ES2097181T3 (en) | 1997-04-01 |
| NO179602B (en) | 1996-08-05 |
| ZA9244B (en) | 1992-10-28 |
| PT99962B (en) | 1999-06-30 |
| NO920056D0 (en) | 1992-01-03 |
| DK0493861T3 (en) | 1997-08-25 |
| JPH05139978A (en) | 1993-06-08 |
| CA2057456A1 (en) | 1992-07-05 |
| NO920056L (en) | 1992-07-06 |
| IE914477A1 (en) | 1992-07-15 |
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