子分类：
| 序号 | 专利名 | 申请号 | 申请日 | 公开（公告）号 | 公开（公告）日 | 发明人 |
|---|---|---|---|---|---|---|
| 81 | Method for modifying and resetting the bloodstream prolactin levels of a human subject | US469012 | 1995-06-05 | US5716957A | 1998-02-10 | Anthony H. Cincotta; Albert H. Meier |
| A process for the long term modification and regulation of lipid and glucose metabolism--generally to reduce obesity, insulin resistance, and hyperinsulinemia or hyperglycemia, or both (these being the hallmarks of noninsulin dependent, or Type II diabetes)--by administration to a vertebrate, animal or human, of a dopamine agonist and a prolactin stimulator. The dopamine agonist and prolactin stimulator are administered in daily dosages, respectively, at a time of day dependent on the normal circadian rhythm of fat and lean members of a similar species. Decreases in body fat deposits result by treatment of an obese species on a daily timed sequence based on circadian rhythms of the peak prolactin, or peak prolactin and peak glucocorticosteroid, blood level established for lean insulin sensitive members of a similar species. The dopamine agonist is administered at the time of, or just after the time of peak plasma prolactin concentration found in lean animals of the same species and the prolactin stimulator is administered at a time just before the plasma prolactin rhythm reaches its peak in lean animals. Insulin resistance, and hyperinsulinemia or hyperglycemia, or both, can also be controlled in humans on a long term basis by treatment corresponding to that of the treatment for obesity. The short term daily injections reset hormonal timing in the neural centers of the brain to produce long term effects. | ||||||
| 82 | Method for the long term reduction of body fat stores, insulin resistance, hypersinsulinemia and hyperglycemia in vertebrates | US249808 | 1994-05-26 | US5554623A | 1996-09-10 | Anthony H. Cincotta; Albert H. Meier |
| A process for the long term modification and regulation of lipid and glucose metabolism--generally to reduce obesity, insulin resistance, and hyperinsulinemia or hyperglycemia, or both (these being the hallmarks of noninsulin dependent, or Type II diabetes)--by administration to a vertebrate, animal or human, of a dopamine agonist and a prolactin stimulator. The dopamine agonist and prolactin stimulator are administered in daily dosages, respectively, at a time of day dependent on the normal circadian rhythm of fat and lean members of a similar species. Decreases in body fat deposits result by treatment of an obese species on a daily timed sequence based on circadian rhythms of the peak prolactin, or peak prolactin and peak glucocorticosteroid, blood level established for lean insulin sensitive members of a similar species. The dopamine agonist is administered at the time of, or just after the time of peak plasma prolactin concentration found in lean animals of the same species and the prolactin stimulator is administered at a time just before the plasma prolactin rhythm reaches its peak in lean animals. Insulin resistance, and hyperinsulinemia or hyperglycemia, or both, can also be controlled in humans on a long term basis by treatment corresponding to that of the treatment for obesity. The short term daily injections reset hormonal timing in the neural centers of the brain to produce long term effects. | ||||||
| 83 | Substituted cyclo or bicycloalkylamides of (8.beta.)-6-(substituted) ergolines | US936684 | 1992-08-27 | US5441961A | 1995-08-15 | Marlene L. Cohen; David W. Robertson |
| The present invention provides (8.beta.)-N-substituted cyclo or bicycloalkyl-6-(substituted)-ergoline-8-carboxamides useful for occupying 5HT.sub.2 or 5HT.sub.1c receptors in mammals. The invention also provides methods for treating a variety of disorders and conditions related to or affecting these receptors as well as pharmaceutical formulations of the compounds of the invention. | ||||||
| 84 | Ergolinyl heterocycles for the treatment of Parkinson's disease and dyskinetic symptoms | US149012 | 1988-01-27 | US4839363A | 1989-06-13 | Enzo Brambilla; Sergio Mantegani; Lorenzo Pegrassi; Alessandro Rossi; Aldemio Temperilli |
| Ergoline derivatives of the formula I ##STR1## wherein R.sub.1 represents a hydrogen atom or a methyl group; R.sub.2 represents a hydrogen atom or a methoxy group;R.sub.3 represents a hydrocarbon group having from 1 to 4 carbon atoms;X represents a nitrogen atom and Y represents an oxygen atom, a ##STR2## group wherein R.sub.4 represents a hydrogen atom, a C.sub.1 -C.sub.4 alkyl or a phenyl group, R.sub.5 represents a hydrogen atom, a C.sub.1 -C.sub.4 alkyl, a phenyl, an amino or di(C.sub.1 -C.sub.4 alkyl)amino group and the nitrogen atom of the group ##STR3## is not joined to the nitrogen atom represented by X, or Y represents a nitrogen atom and X represents an oxygen atom or a ##STR4## group wherein R.sub.4 is as above defined; and the pharmaceutically acceptable salt thereof; are useful for treatment of Parkinsonism and dyskinetic symptoms. | ||||||
| 85 | Process for the production of ergot alkaloids | US357526 | 1982-03-12 | US4491664A | 1985-01-01 | Wolfgang Oppolzer |
| A process for the production of an ergot alkaloid comprising intramolecularly cyclizing a 3-iminoethyl-4-trans-buta-1',3'-dienylindole to produce an 8-ergolene and as necessary converting the resultant ergolene into the desired ergot alkaloid. | ||||||
| 86 | SLOW-RELEASE CONJUGATES OF SN-38 | PCT/US2014/059146 | 2014-10-03 | WO2015051307A1 | 2015-04-09 | ASHLEY, Gary; SCHNEIDER, Eric L. |
Conjugates of SN-38 that provide optimal drug release rates and minimize the formation of the corresponding glucuronate are described. The conjugates release SN-38 from a polyethylene glycol through a β-elimination mechanism. |
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| 87 | NOVEL FLUOROERGOLINE ANALOGS | PCT/US2012/043677 | 2012-06-22 | WO2012177962A1 | 2012-12-27 | COOK, Robert, O.; ZHANG, Jian; ARMER, Thomas, A. |
Provided herein are novel fluoroergoline derivatives and compositions thereof. In other embodiments, provided herein are methods of treatment, prevention, or amelioration of a variety of medical disorders such as, for example, migraine using the compounds and compositions disclosed herein. In still other embodiments, provided herein are methods of agonizing receptors such as, for example, the 5-HTiD and/or the 5-HT1B receptor, without agonizing the 5-HT2B receptor using the compounds and composittons disclosed herein. In still other embodiments, provided herein are methods of antagonizing or inhibiting activity at receptors such as, for example, the adrenergic alpha2A and/or the alpha2B receptors using the compounds and compositions disclosed herein. |
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| 88 | ERGOLINE DERIVATIVES AS SELECTIVE RADICAL SCAVENGERS FOR NEURONS | PCT/EP2008/066748 | 2008-12-04 | WO2009071607A2 | 2009-06-11 | FLIEGER, Miroslav; KRANDA, Karel; LATTÉ, Klaus Peter; PERTZ, Heinz Helmut; HOROWSKI, Reinhard |
The present invention relates to new Ergot alkaloid derivatives of the general formula (I) or pharmaceutically acceptable salts thereof as well as to the use of specific compounds as selective radical scavengers for neurons. |
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| 89 | PROCESS FOR THE MANUFACTURE OF LYSERGIC ACID | PCT/US2005/004933 | 2005-02-17 | WO2005082902A1 | 2005-09-09 | CVAK, Ladislav; MOJCZEK, Vlastislav |
Lysergic acid is formed in high yields and high quality by isomerizing paspalic acid in a phase separated mixture formed by paspalic acid and a concentrated aqueous metal hydroxide solution. |
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| 90 | TRANSDERMAL THERAPEUTIC SYSTEM | PCT/EP2001/009824 | 2001-08-24 | WO02015890A1 | 2002-02-28 | |
| The invention relates to a use of a transdermal therapeutic system (TTS) for producing an agent for obtaining and maintaining the circadian rhythm under dopamine therapy. Said system comprises a pharmaceutical layer containing at least one matrix having an active ingredient; and/or an active ingredient reservoir; a diffusion barrier which is permeable to active ingredients and which is arranged on the skin side of the active ingredient reservoir; and an ergoline derivative or salt thereof having a physiologically compatible acid, as an active ingredient. | ||||||
| 91 | SLOW-RELEASE CONJUGATES OF SN-38 | US16009078 | 2018-06-14 | US20180289695A1 | 2018-10-11 | Gary W. ASHLEY; Eric L. SCHNEIDER |
| Conjugates of SN-38 that provide optimal drug release rates and minimize the formation of the corresponding glucuronate are described. The conjugates release SN-38 from a polyethylene glycol through a β-elimination mechanism. | ||||||
| 92 | [1,2,4] triazol [1,5-a] pyrazines useful as inhibitors of phosphodiesterases | US13347541 | 2012-01-10 | US08765760B2 | 2014-07-01 | John Emmerson Campbell; Philip Jones; Michael Charles Hewitt |
| Provided herein are compounds of formula (I): A-L-B (I) and pharmaceutically acceptable salts and stereoisomers thereof, wherein A is wherein X is (i) CR1 or N, or (ii) O or NR2, each Y is independently N or CR3, and each Z is independently N or C, wherein R1, R2 and R3 are defined in the specification; L is a linker, and B is a multicyclic ring; methods of their synthesis, pharmaceutical compositions comprising the compounds, and methods of their use. The compounds provided herein are inhibitors of phosphodiesterases and useful for the treatment, prevention, and/or management of various disorders, such as CNS disorders and metabolic disorders, e.g., neurological disorders, psychosis, schizophrenia, obesity and diabetes. | ||||||
| 93 | Crystal form of cabergoline | US12525240 | 2008-01-30 | US08338445B2 | 2012-12-25 | Zoran Ham; Andrej Premrl |
| The present invention relates to a cabergoline crystal form L, its preparation from halogenated aromatic solvents and aliphatic hydrocarbons and to pharmaceutical compositions containing the new form. | ||||||
| 94 | CRYSTAL FORM OF CABERGOLINE | US12525240 | 2008-01-30 | US20100152223A1 | 2010-06-17 | Zoran Ham; Andrej Premrl |
| The present invention relates to a cabergoline crystal form L, its preparation from halogenated aromatic solvents and aliphatic hydrocarbons and to pharmaceutical compositions containing the new form. | ||||||
| 95 | Preparation of cabergoline | US11060991 | 2005-02-18 | US07186837B2 | 2007-03-06 | Alan Greenwood; Derek McHattie; Parveen Bhatarah; Mark Philip Gamble |
| The present invention discloses a method for preparing cabergoline form I by combining cabergoline and a solvent comprising ethylbenzene to form a solvate and obtaining form I from the solvate. Also disclosed in a method for preparing cabergoline form I by combining cabergoline and a first solvent to form a solution and additionally including a second solvent to the solution, followed by crystallization to form cabergoline form I. Further disclosed is a solvate form of cabergoline comprising cabergoline and ethylbenzene and, optionally, n-heptane. | ||||||
| 96 | Haptens, immunogens, antibodies and conjugates to 2-oxo-3-hydroxy-LSD | US10326771 | 2002-12-20 | US07115718B2 | 2006-10-03 | Robert Ivan McConnell; Elouard Benchikh; Stephen Peter Fitzgerald; John Victor Lamont |
| The invention provides a hapten derivatized with a crosslinker at the nitrogen of the 8β-carboxamide of 2-oxo-3-hydroxy LSD. The invention also provides an immunogen comprising the aforementioned hapten coupled to an antigenicity-conferring carrier material; a conjugate comprising the aforementioned hapten coupled to a labelling agent, as well as, antibodies raised against the aforementioned immunogen and capable of binding with at least the 3-hydroxy-2-pyrrolidone structural epitope of 2-oxo-3-hydroxy LSD. | ||||||
| 97 | Therapeutic process for the treatment of the pathologies of type II diabetes | US465818 | 1995-06-06 | US5866584A | 1999-02-02 | Anthony H. Cincotta; Albert H. Meier |
| A process for the long term modification and regulation of lipid and carbohydrate metabolism--generally to reduce obesity, insulin resistance, and hyperinsulinemia or hyperglycemia, or both (these are the hallmarks of noninsulin dependent, or Type II diabetes)--by administration (i.e., by oral, sublingual or parenternal administration) to a vertebrate, animal or human, of a dopamine agonist, e.g., bromocriptine. Administration of the bromocriptine is made over a limited period at a time of day dependent on the normal circadian rhythm of insulin resistant and insulin sensitive members of a similar species. Insulin resistance, and hyperinsulinemia and hyperglycemia, or both, can be controlled in humans on a long term basis by such treatment inasmuch as the short term, daily administration resets hormonal timing in the neural centers of the brain to produce long term effects. | ||||||
| 98 | Therapeutic package for the long term reduction of body fat stores insulin resistance hyperinsulinemia and hyperglycemia in vertebrates | US843760 | 1997-04-21 | US5854255A | 1998-12-29 | Anthony H. Cincotta; Albert H. Meier |
| A therapeutic package for dispensing to, or for use in dispensing to, a vertebrate being treated for a metabolic condition selected from the group consisting of obesity, insulin resistance, hyperinsulinemia, and hyperglycemia comprising one or more unit doses of bromocriptine and labeling directing the use of the package in the treatment of the metabolic condition in a dosage regimen under which the delivery of the bromocriptine is confined to the period during the day near the time of day at which the serum prolactin concentration of a lean, insulin sensitive vertebrate of the same sex is low, and further directing the use of said package in conjunction with the concomitant administration to the vertebrate of one or more unit doses providing a therapeutically effective amount of a prolactin stimulator in a dosage regimen under which the delivery of the prolactin stimulator is confined to the period during the day after the time at which the serum prolactin concentration of a lean, insulin-sensitive vertebrate of the same sex reaches its lowest point and prior to the time of day when the prolactin concentration rises to a peak in lean, insulin-sensitive vertebrates of the same sex. | ||||||
| 99 | Method for modifying or regulating the glucose metabolism of an animal or human subject | US465674 | 1995-06-06 | US5654313A | 1997-08-05 | Anthony H. Cincotta; Albert H. Meier |
| A process for the long term modification and regulation of lipid and glucose metabolism--generally to reduce obesity, insulin resistance, and hyperinsulinemia or hyperglycemia, or both (these being the hallmarks of noninsulin dependent, or Type II diabetes)--by administration to a vertebrate, animal or human, of a dopamine agonist and a prolactin stimulator. The dopamine agonist and prolactin stimulator are administered in daily dosages, respectively, at a time of day dependent on the normal circadian rhythm of fat and lean members of a similar species. Decreases in body fat deposits result by treatment of an obese species on a daily timed sequence based on circadian rhythms of the peak prolactin, or peak prolactin and peak glucocorticosteroid, blood level established for lean insulin sensitive members of a similar species. The dopamine agonist is administered at the time of, or just after the time of peak plasma prolactin concentration found in lean animals of the same species and the prolactin stimulator is administered at a time just before the plasma prolactin rhythm reaches its peak in lean animals. Insulin resistance, and hyperinsulinemia or hyperglycemia, or both, can also be controlled in humans on a long term basis by treatment corresponding to that of the treatment for obesity. The short term daily injections reset hormonal timing in the neural centers of the brain to produce long term effects. | ||||||
| 100 | Process for the long term reduction of body fat stores, insulin resistance, hyperinsulinemia in vertebrates | US287066 | 1994-08-08 | US5496803A | 1996-03-05 | Albert H. Meier; Anthony H. Cincotta |
| A process for the long-term modification and regulation of lipid metabolism--generally to reduce obesity, insulin resistance, and hyperinsulinemia (the three hallmarks of Type II diabetes)--by injections into the bloodstream of a vertebrate, animal or human, of prolactin, or both prolactin and a glucocorticosteroid. The injections are made over a limited period at a time of day dependent on the normal circadian rhythm of fat and lean members of a similar species. Decreases (or increases) in body fat deposits result by treatment of an obese species (lean species) on a daily timed sequence based on circadian rhythms of the peak prolactin, or peak prolactin and peak glucocorticosteroid, blood level established for lean members (or obese members) of a similar species. Insulin resistance, and hyperinsulinemia can also be controlled in humans on a long-term basis by treatment corresponding to that of the treatment for obesity. The short-term daily injections reset hormonal timing in the neural centers of the brain to produce long-term effects. | ||||||
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