DOCSLIB.ORG

Apomorphine (APO-Go)

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text

Load more

SUMMARY SHEET FOR Apomorphine (APO-go) For the treatment of Parkinson's disease Licensed indication agonists are no longer effective or poorly tolerated, it may be necessary to use apomorphine. The treatment of disabling motor fluctuations in patients with Parkinson's disease which persist after treatment Dosage and administration with levodopa (with a peripheral decarboxylase inhibitor) Apomorphine is administered by the subcutaneous (SC) and/or other dopamine agonists.1,2 route. It is available as ampoules for injection and as a Apomorphine should be initiated in the controlled prefilled pen-injector, all of the same strength (10mg/ml). environment of a specialist clinic.1,2 The patient should Full details on initiating treatment are given in the be assessed/treatment supervised by a physician Summary of Product Characteristics (SPC).1,2 Prior to experienced in the treatment of Parkinson's disease. The initiating apomorphine treatment, patients should be patients’ treatment with levodopa and/or dopamine established on domperidone (usually 20mg three time a agonists should be optimised before starting apomorphine day) for at least 2 days. The optimum dose of treatment. apomorphine needs to be determined on an individual Background information patient basis. During continuing treatment the daily dose varies widely between patients and is typically within the Parkinson’s disease (PD) is a progressive neurological range 3-30mg, with each dose administered at the start of disorder characterised by tremor, bradykinesia, rigidity 3 an 'off' episode. Individual bolus injections and the total and postural disturbances. The disease results from the daily dose should not exceed 10mg and 100mg degeneration of dopaminergic neurones in the substantia respectively. nigra of the midbrain. For patients whose overall control remains unsatisfactory Current treatment options using intermittent injections, or who require many and Diagnosis is made on clinical grounds and should be frequent injections (>10 per day), apomorphine can be undertaken by a specialist. Treatment of PD is administered as a continuous SC infusion. symptomatic, as there is insufficient evidence of the effect Patients selected for treatment with the pen-injector should 4 of any agent on disease progression. Treatment should be able to recognise the onset of their 'off' symptoms and be be started when there is significant functional disability capable of injecting themselves, or have a responsible carer affecting activities of daily living. able to inject for them when required. Levodopa, used in conjunction with a dopa-decarboxylase Clinical efficacy inhibitor has been the mainstay of treatment in PD although dopamine agonists are now being used in the There is a lack of good quality published trials for treatment of early disease,4 particularly in younger apomorphine in the treatment of motor fluctuations in patients. It is believed that use of dopamine agonists (e.g. Parkinson's disease. Several studies have been conducted ropinirole, pramipexole, pergolide) at this stage may in small groups of patients, most of which have been open, delay the long-term adverse effects of levodopa e.g. non-comparative investigations or observations with dyskinesias. subjective end points. These studies collectively recorded a reduction in 'off' time of 50-85% with apomorphine Traditional treatment with levodopa can be anticipated to administered for periods of 6 months to 2 years. 6,7 control symptoms throughout the day during the first few years of therapy. Within 3-5 years of initiating treatment Data from short-term randomised controlled studies, where at least half of patients develop fluctuations in response apomorphine was administered by intermittent SC with dyskinesia and end-of-dose akinesia or ‘wearing injection, show: off’.5 Additionally the swing from mobility to immobility · a >50% reduction in 'off' time with apomorphine (vs (the ‘on-off’ effect) can become more frequent and placebo)8 abrupt. · that a significantly greater proportion of 'off' episodes were aborted with apomorphine compared with As PD progresses, adjustment of medication by addition placebo (95% vs 23% p<0.001)9 of adjunctive agents (e.g. entacapone, dopamine agonists, selegiline), or increasing the dose of levodopa, increasing Longer-term observational studies have also been the frequency of levodopa dosing, or using a slow release published, where apomorphine was administered by SC preparation of levodopa is usually required.3 In the later infusion during waking hours or by intermittent SC stages of the disease when levodopa and dopamine injection for periods of 3 months to 9 years.10-13 These data show that the reduction in the number of 'off' periods Parkinson's disease. Data from small, short-term or time in 'off' state was sustained over the longer term. randomised controlled studies show a ³50% reduction in In many patients levodopa dosage was reduced or 'off' time with apomorphine, which appears to be treatment withdrawn when concomitant apomorphine was maintained over the longer-term (observational data). introduced.11,13 Varying effects on patients' dyskinetic episodes were seen in these studies, from little if any The most common adverse effects seen with apomorphine overall change in intensity or duration of episodes,12 to are nausea, vomiting, and nodules or indurations at the reduced disability,11 or increasingly severe 'on' phase injection site. In some patients dyskinetic episodes may dyskinesia.10 occur which can be severe. Two small (n=6, 20) comparative studies with lisuride Careful introduction of apomorphine treatment is infusion have been published. These studies were too required, which necessitates hospital initiation. small to demonstrate any significant differences.14,15 References 1 Britannia Pharmaceuticals Ltd. APO-go ampoules. Summary of Adverse effects Product Characteristics 2000. 2 Britannia Pharmaceuticals Ltd. APO-go PEN 10mg/ml. Summary Nausea, vomiting and local indurations/nodules at of Product Characteristics 2001. subcutaneous injection sites are the most common side 3 Thomson F, Muir A, Stirton J, Macphee G, Hudson S. Parkinson's Disease. Pharm J 2001;267:600-12. effects. The local SC effects may be reduced in some cases 4 Bhatia K, Brooks DJ, Burn DJ, et al. Updated guidelines for the by rotation of injection sites, dilution of the solution with management of Parkinson's disease. Hospital Medicine 0.9% sodium chloride, and possibly the use of ultrasound to 2001;62:456-70. areas of nodularity and induration. 5 Quinn N. Drug treatment of Parkinsons's disease. BMJ 1995;310:575-9. Nausea, vomiting and local indurations/nodules at 6 Stibe CMH et al. Subcutaneous Apomorphine in Parkinsonian On- Off Oscillations Lancet 1988;i;403-406. subcutaneous injection sites are the most common side 7 Corboy DL, Wagner ML, Sage JI. Apomorphine for Motor effects. Dyskinesias can occur during 'on' periods which Fluctuations and Freezing in Parkinson's Disease Ann Pharmacother can be severe, leading to withdrawal of treatment in some 1995;29:282-8. patients. Other adverse events include neuropsychiatric 8 Ostergaard L, et al. Pen injected apomorphine against off phenomena in late Parkinson's disease: a double blind, placebo disturbances, transient sedation, and hypotension. controlled study. J Neurol Neurosurg Psychiatry 1995;58:681-7. 9 Dewey RB, et al. A randomized, double-blind, placebo-controlled trial of subcutaneously injected apomorphine for Parkinsonian off- Costs state events. Arch Neurol 2001;58:1385-92. 10 Hughes A.J. Subcutaneous Apomorphine in Parkinson's Disease: At current prices treatment with apomorphine 10mg/ml Response to Chronic Administration for up to Five Years. Movement costs: Disorders 1993;8:165-170. · £37.96 for 5x2ml ampoules 11 Colzi A, Turner K, Lees AJ. Continuous subcutaneous waking day apomorphine in the long term treatment of levodopa induced · £76.16 for 5x5ml ampoules interdose dyskinesias in Parkinson's disease. J Neurol Neurosurg · £123.91 for 5x3ml pens Psychiatry 1998;64:573-6. 12 Pietz K, Hagell P, Odin P. Subcutaneous apomorphine in late stage Summary Parkinson's disease: a long term follow up. J Neurol Neurosurg Psychiatry 1998;65:709-16. Apomorphine is a dopamine agonist available as a 13 Gancher ST, et al. Apomorphine infusional therapy in Parkinson's parenteral preparation, used in the later stages of disease: clinical utility and lack of tolerance. Movement Disorders 1995;10:37-43. Parkinson's disease to treat disabling motor fluctuations 14 Stocci F et al. Apomorphine and lisuride infusion: a comparative which persist despite optimal treatment with levodopa chronic study. Adv Neurol 1993;60:653-5. and/or dopamine agonists. 15 Stibe C, Lees A, Stern G. Subcutaneous infusion of apomorphine and lisuride in the treatment of Parkinsonian on-off fluctuations. There is a paucity of good quality clinical trial data on Lancet 1987;i:871. apomorphine for the treatment of motor fluctuations in Date: November 2002 ©Midland Therapeutic Review & Advisory Committee, SS02/21 Department of Medicines Management (THIS SUMMARY SHEET REPLACES 95/03) .
Recommended publications
  • Pericardial, Retroperitoneal, and Pleural Fibrosis Induced by Pergolide

    Pericardial, Retroperitoneal, and Pleural Fibrosis Induced by Pergolide

    J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.66.1.79 on 1 January 1999. Downloaded from J Neurol Neurosurg Psychiatry 1999;66:79–81 79 SHORT REPORT Pericardial, retroperitoneal, and pleural fibrosis induced by pergolide S Shaunak, A Wilkins, J B Pilling, D J Dick Abstract 1992, the emergence of motor fluctuations led Three patients with Parkinson’s disease to the introduction of pergolide, and the dose are described who developed pericardial, of this was gradually increased to a maximum retroperitoneal, and pleural fibrosis asso- of 1mg/day. 1n 1994, 2 years after the ciated with pergolide treatment. Surgical introduction of pergolide, the patient devel- intervention was required in all three oped left flank pain with weight loss, and was cases, either to reach a tissue diagnosis or found to have a mild anaemia (haemoglobin for potentially life threatening complica- 10.4 g/dl), with indices suggesting iron defi- tions. Symptoms emerged on average 2 ciency, and an ESR of 40 mm/h. Upper gastro- years after the institution of treatment, intestinal endoscopy and barium enema gave and were suYciently non-specific to cause negative results. Seven months later right sided significant delays in diagnosis in all cases. chest pain and a non-productive cough devel- The erythrocyte sedimentation rate (ESR) oped; investigations confirmed persistent anae- was raised in the two patients in whom it mia, an ESR of 55 mm/h, and bilateral pleural was measured. Serosal fibrosis is a rarely thickening on chest radiography and CT. Lung reported adverse eVect of pergolide treat- function tests showed a reduction in total lung ment, although it is well described with capacity of 36% with no fall in transfer factor, other dopamine agonists.
  • Evidence from Horses with Pituitary Pars Intermedia Dysfunction Jessica S

    Evidence from Horses with Pituitary Pars Intermedia Dysfunction Jessica S

    Fortin et al. BMC Veterinary Research (2020) 16:356 https://doi.org/10.1186/s12917-020-02565-3 RESEARCH ARTICLE Open Access Restoring pars intermedia dopamine concentrations and tyrosine hydroxylase expression levels with pergolide: evidence from horses with pituitary pars intermedia dysfunction Jessica S. Fortin1*, Matthew J. Benskey2, Keith J. Lookingland2, Jon S. Patterson1, Erin B. Howey1, John L. Goudreau2,3 and Harold C. Schott II4* Abstract Background: Pituitary pars intermedia dysfunction (PPID) develops slowly in aged horses as degeneration of hypothalamic dopaminergic neurons leads to proliferation of pars intermedia (PI) melanotropes through hyperplasia and adenoma formation. Dopamine (DA) concentrations and tyrosine hydroxylase (TH) immunoreactivity are markedly reduced in PI tissue of PPID-affected equids and treatment with the DA receptor agonist pergolide results in notable clinical improvement. Thus, we hypothesized that pergolide treatment of PPID-affected horses would result in greater DA and TH levels in PI tissue collected from PPID-affected horses versus untreated PPID-affected horses. To test this hypothesis, pituitary glands were removed from 18 horses: four untreated PPID-affected horses, four aged and four young horses without signs of PPID, and six PPID-affected horses that had been treated with pergolide at 2 µg/kg orally once daily for 6 months. DA concentrations and TH expression levels in PI tissues were determined by high performance liquid chromatography with electrochemical detection and Western blot analyses, respectively. Results: DA and TH levels were lowest in PI collected from untreated PPID-affected horses while levels in the pergolide treated horses were similar to those of aged horses without signs of PPID.
  • WO 2014/106238 Al 3 July 2014 (03.07.2014) P O P C T

    WO 2014/106238 Al 3 July 2014 (03.07.2014) P O P C T

    (12) INTERNATIONAL APPLICATION PUBLISHED UNDER THE PATENT COOPERATION TREATY (PCT) (19) World Intellectual Property Organization International Bureau (10) International Publication Number (43) International Publication Date WO 2014/106238 Al 3 July 2014 (03.07.2014) P O P C T (51) International Patent Classification: AO, AT, AU, AZ, BA, BB, BG, BH, BN, BR, BW, BY, A61K 31/404 (2006.01) C07D 209/04 (2006.01) BZ, CA, CH, CL, CN, CO, CR, CU, CZ, DE, DK, DM, A61P 25/18 (2006.01) DO, DZ, EC, EE, EG, ES, FI, GB, GD, GE, GH, GM, GT, HN, HR, HU, ID, IL, IN, IR, IS, JP, KE, KG, KN, KP, KR, (21) International Application Number: KZ, LA, LC, LK, LR, LS, LT, LU, LY, MA, MD, ME, PCT/US2013/078453 MG, MK, MN, MW, MX, MY, MZ, NA, NG, NI, NO, NZ, (22) International Filing Date: OM, PA, PE, PG, PH, PL, PT, QA, RO, RS, RU, RW, SA, 3 1 December 2013 (3 1.12.2013) SC, SD, SE, SG, SK, SL, SM, ST, SV, SY, TH, TJ, TM, TN, TR, TT, TZ, UA, UG, US, UZ, VC, VN, ZA, ZM, (25) Filing Language: English ZW. (26) Publication Language: English (84) Designated States (unless otherwise indicated, for every (30) Priority Data: kind of regional protection available): ARIPO (BW, GH, 61/747,499 31 December 2012 (3 1. 12.2012) US GM, KE, LR, LS, MW, MZ, NA, RW, SD, SL, SZ, TZ, UG, ZM, ZW), Eurasian (AM, AZ, BY, KG, KZ, RU, TJ, (71) Applicant: FANG, Qun, Kevin [US/US]; 34 Atwood TM), European (AL, AT, BE, BG, CH, CY, CZ, DE, DK, Street, Westfield, MA 02482 (US).
  • Progress and Prospects of Ergot Alkaloid Research

    Progress and Prospects of Ergot Alkaloid Research

    Progress and Prospects of Ergot Alkaloid Research Joydeep Mukherjee, Miriam Menge Institut für Technische Chemie, Universität Hannover, Callinstr. 3, D-30167 Hannover, Germany E-mail: [email protected] Ergot alkaloids, produced by the plant parasitic fungi Claviceps purpurea are important pharmaceuticals. The chemistry, biosynthesis, bioconversions, physiological controls, and biochemistry have been extensively reviewed by earlier authors.We present here the research done on the organic synthesis of the ergot alkaloids during the past two decades. Our aim is to apply this knowledge to the synthesis of novel synthons and thus obtain new molecules by directed biosynthesis. The synthesis of clavine alkaloids, lysergic acid derivatives, the use of tryptophan as the starting material, the chemistry of 1,3,4,5-tetrahydrobenzo[cd]indoles, and the structure activity relationships for ergot alkaloids have been discussed. Recent advances in the molecular biology and enzymology of the fungus are also mentioned. Application of oxygen vectors and mathematical modeling in the large scale production of the alkaloids are also discussed. Finally, the review gives an overview of the use of modern analytical methods such as capillary electrophoresis and two-dimensional fluorescence spectroscopy. Keywords. Ergot, Alkaloid synthesis, Claviceps, Directed biosynthesis, Bioreactors 1Introduction . 2 2 Chemistry, Bioconversions, and Directed Biosynthesis . 2 2.1 Chemical Synthesis . 3 2.1.1 Chemical Structures . 3 2.1.1.1 Clavine Alkaloids . 3 2.1.1.2 Simple Lysergic Acid Derivatives . 4 2.1.1.3 Ergopeptines . 4 2.1.1.4 Ergopeptams . 5 2.1.2 Synthesis of Clavine Alkaloids and Lysergic Acid Derivatives . 5 2.1.3 Use of Tryptophan as the Starting Material .
  • Biased Ligands Differentially Shape the Conformation of The

    Biased Ligands Differentially Shape the Conformation of The

    International Journal of Molecular Sciences Article Biased Ligands Differentially Shape the Conformation of the Extracellular Loop Region in 5-HT2B Receptors Katrin Denzinger, Trung Ngoc Nguyen, Theresa Noonan, Gerhard Wolber and Marcel Bermudez * Institute of Pharmacy, Freie Universität Berlin, Königin-Luise-Strasse 2-4, 14195 Berlin, Germany; [email protected] (K.D.); [email protected] (T.N.N.); [email protected] (T.N.); [email protected] (G.W.) * Correspondence: [email protected] Received: 22 November 2020; Accepted: 18 December 2020; Published: 20 December 2020 Abstract: G protein-coupled receptors are linked to various intracellular transducers, each pathway associated with different physiological effects. Biased ligands, capable of activating one pathway over another, are gaining attention for their therapeutic potential, as they could selectively activate beneficial pathways whilst avoiding those responsible for adverse effects. We performed molecular dynamics simulations with known β-arrestin-biased ligands like lysergic acid diethylamide and ergotamine in complex with the 5-HT2B receptor and discovered that the extent of ligand bias is directly connected with the degree of closure of the extracellular loop region. Given a loose allosteric coupling of extracellular and intracellular receptor regions, we delineate a concept for biased signaling at serotonin receptors, by which conformational interference with binding pocket closure restricts the signaling repertoire of the receptor. Molecular docking studies of biased ligands gathered from the BiasDB demonstrate that larger ligands only show plausible docking poses in the ergotamine-bound structure, highlighting the conformational constraints associated with bias. This emphasizes the importance of selecting the appropriate receptor conformation on which to base virtual screening workflows in structure-based drug design of biased ligands.
  • Prascend® (Pergolide Tablets)1 Mg

    Prascend® (Pergolide Tablets)1 Mg

    PRASCEND- pergolide tablet Boehringer Ingelheim Animal Health USA Inc. ---------- Prascend® (pergolide tablets) 1 mg Dopamine receptor agonist for oral use in horses only Caution: Federal law restricts this drug to use by or on the order of a licensed veterinarian. Description: PRASCEND Tablets are rectangular light red colored, half-scored tablets containing 1 mg pergolide, as pergolide mesylate. Pergolide mesylate is a synthetic ergot derivative and is a potent dopamine receptor agonist. The chemical name of pergolide mesylate is 8β-[(Methylthio) methyl]-6- propylergoline monomethanesulfonate. The chemical structure is: Indication: For the control of clinical signs associated with Pituitary Pars Intermedia Dysfunction (Equine Cushing’s Disease) in horses. Dosage and Administration: Administer orally at a starting dose of 2 mcg/kg once daily. Dosage may be adjusted to effect, not to exceed 4 mcg/kg daily. It has been reported that pergolide tablets may cause eye irritation, an irritating smell, or headache when PRASCEND Tablets are split or crushed. PRASCEND Tablets should not be crushed due to the potential for increased human exposure and care should be taken to minimize exposure when splitting tablets. The tablets are scored and the calculated dosage should be provided to the nearest one-half tablet increment (see Table 1). Table 1 Dosing Table Dosage Dosage Body Weight 2 mcg/kg 4 mcg/kg 136 - 340 kg 0.5 tablet 1 tablet (300 - 749 lb) 341 - 567 kg 1 tablet 2 tablets (750 - 1,249 lb) 568 - 795 kg 1.5 tablets 3 tablets (1,250 - 1,749 lb) 796 - 1,022 kg 2 tablets 4 tablets (1,750 - 2,249 lb) Dosing should be titrated according to individual response to therapy to achieve the lowest effective dose.
  • WO 2010/099522 Al

    WO 2010/099522 Al

    (12) INTERNATIONAL APPLICATION PUBLISHED UNDER THE PATENT COOPERATION TREATY (PCT) (19) World Intellectual Property Organization International Bureau (10) International Publication Number (43) International Publication Date 2 September 2010 (02.09.2010) WO 2010/099522 Al (51) International Patent Classification: (81) Designated States (unless otherwise indicated, for every A61K 45/06 (2006.01) A61K 31/4164 (2006.01) kind of national protection available): AE, AG, AL, AM, A61K 31/4045 (2006.01) A61K 31/00 (2006.01) AO, AT, AU, AZ, BA, BB, BG, BH, BR, BW, BY, BZ, CA, CH, CL, CN, CO, CR, CU, CZ, DE, DK, DM, DO, (21) International Application Number: DZ, EC, EE, EG, ES, FI, GB, GD, GE, GH, GM, GT, PCT/US2010/025725 HN, HR, HU, ID, IL, IN, IS, JP, KE, KG, KM, KN, KP, (22) International Filing Date: KR, KZ, LA, LC, LK, LR, LS, LT, LU, LY, MA, MD, 1 March 2010 (01 .03.2010) ME, MG, MK, MN, MW, MX, MY, MZ, NA, NG, NI, NO, NZ, OM, PE, PG, PH, PL, PT, RO, RS, RU, SC, SD, (25) Filing Language: English SE, SG, SK, SL, SM, ST, SV, SY, TH, TJ, TM, TN, TR, (26) Publication Language: English TT, TZ, UA, UG, US, UZ, VC, VN, ZA, ZM, ZW. (30) Priority Data: (84) Designated States (unless otherwise indicated, for every 61/156,129 27 February 2009 (27.02.2009) US kind of regional protection available): ARIPO (BW, GH, GM, KE, LS, MW, MZ, NA, SD, SL, SZ, TZ, UG, ZM, (71) Applicant (for all designated States except US): ZW), Eurasian (AM, AZ, BY, KG, KZ, MD, RU, TJ, HELSINN THERAPEUTICS (U.S.), INC.
  • Summary of Product Characteristics

    Summary of Product Characteristics

    Health Products Regulatory Authority Summary of Product Characteristics 1 NAME OF THE MEDICINAL PRODUCT Zirtek Plus Decongestant 5mg/120mg Prolonged Release Tablet 2 QUALITATIVE AND QUANTITATIVE COMPOSITION Each tablet provides 5 mg cetirizine dihydrochloride for immediate release, and 120 mg pseudoephedrine hydrochloride for prolonged release. Excipients with known effect: one tablet contains 43.23 mg lactose monohydrate For the full list of excipients, see section 6.1 3 PHARMACEUTICAL FORM Prolonged release tablet. White to off-white, round, biconvex circle-embossed, film-coated tablet, having a circular logo on one side. 4 CLINICAL PARTICULARS 4.1 Therapeutic Indications Cetirizine-pseudoephedrine is indicated for the treatment of symptoms such as nasal congestion, sneezing, rhinorrhoea, and nasal and ocular pruritus associated with seasonal or perennial allergic rhinitis. Cetirizine-pseudoephedrine should be administered when the anti-allergic properties of cetirizine dihydrochloride and the nasal decongestant activity of pseudoephedrine hydrochloride are desired. 4.2 Posology and method of administration Posology Adults One tablet two times a day (morning and evening), corresponding to the maximum recommended dose of 10 mg of cetirizine dihydrochloride and 240 mg of pseudoephedrine hydrochloride daily. Special populations Paediatric population Adolescents from 12 years of age and above: 1 tablet two times a day (morning and evening), with or without food. Children under 12 years of age: the use of the product is contraindicated (see sections 4.3 and 4.4). Renal impairment The dose should be reduced to 1 tablet daily in patients with moderate renal insufficiency. Hepatic impairment The dose should be reduced to 1 tablet daily in patients with moderate hepatic insufficiency.
  • USP Reference Standards Catalog

    USP Reference Standards Catalog

    Last Updated On: January 6, 2016 USP Reference Standards Catalog Catalog # Description Current Lot Previous Lot CAS # NDC # Unit Price Special Restriction 1000408 Abacavir Sulfate R028L0 F1L487 (12/16) 188062-50-2 $222.00 (200 mg) 1000419 Abacavir Sulfate F0G248 188062-50-2 $692.00 Racemic (20 mg) (4-[2-amino-6-(cyclo propylamino)-9H-pur in-9yl]-2-cyclopenten e-1-methanol sulfate (2:1)) 1000420 Abacavir Related F1L311 F0H284 (10/13) 124752-25-6 $692.00 Compound A (20 mg) ([4-(2,6-diamino-9H- purin-9-yl)cyclopent- 2-enyl]methanol) 1000437 Abacavir Related F0M143 N/A $692.00 Compound D (20 mg) (N6-Cyclopropyl-9-{( 1R,4S)-4-[(2,5-diami no-6-chlorpyrimidin- 4-yloxy)methyl] cyclopent-2-enyl}-9H -purine-2,6-diamine) 1000441 Abacavir Related F1L318 F0H283 (10/13) N/A $692.00 Compound B (20 mg) ([4-(2,5-diamino-6-c Page 1 Last Updated On: January 6, 2016 USP Reference Standards Catalog Catalog # Description Current Lot Previous Lot CAS # NDC # Unit Price Special Restriction hloropyrimidin-4-yla mino)cyclopent-2-en yl]methanol) 1000452 Abacavir Related F1L322 F0H285 (09/13) 172015-79-1 $692.00 Compound C (20 mg) ([(1S,4R)-4-(2-amino -6-chloro-9H-purin-9 -yl)cyclopent-2-enyl] methanol hydrochloride) 1000485 Abacavir Related R039P0 F0J094 (11/16) N/A $692.00 Compounds Mixture (15 mg) 1000496 Abacavir F0J102 N/A $692.00 Stereoisomers Mixture (15 mg) 1000500 Abacavir System F0J097 N/A $692.00 Suitability Mixture (15 mg) 1000521 Acarbose (200 mg) F0M160 56180-94-0 $222.00 (COLD SHIPMENT REQUIRED) 1000532 Acarbose System F0L204 N/A $692.00 Suitability
  • Effect of Dietary Exposure to Ergot Alkaloids on Contractility of Bovine Mesenteric Vasculature and Rumen Motility

    Effect of Dietary Exposure to Ergot Alkaloids on Contractility of Bovine Mesenteric Vasculature and Rumen Motility

    University of Kentucky UKnowledge Theses and Dissertations--Animal and Food Sciences Animal and Food Sciences 2014 EFFECT OF DIETARY EXPOSURE TO ERGOT ALKALOIDS ON CONTRACTILITY OF BOVINE MESENTERIC VASCULATURE AND RUMEN MOTILITY Amanda M. Egert University of Kentucky, [email protected] Right click to open a feedback form in a new tab to let us know how this document benefits ou.y Recommended Citation Egert, Amanda M., "EFFECT OF DIETARY EXPOSURE TO ERGOT ALKALOIDS ON CONTRACTILITY OF BOVINE MESENTERIC VASCULATURE AND RUMEN MOTILITY" (2014). Theses and Dissertations--Animal and Food Sciences. 40. https://uknowledge.uky.edu/animalsci_etds/40 This Master's Thesis is brought to you for free and open access by the Animal and Food Sciences at UKnowledge. It has been accepted for inclusion in Theses and Dissertations--Animal and Food Sciences by an authorized administrator of UKnowledge. For more information, please contact [email protected]. STUDENT AGREEMENT: I represent that my thesis or dissertation and abstract are my original work. Proper attribution has been given to all outside sources. I understand that I am solely responsible for obtaining any needed copyright permissions. I have obtained needed written permission statement(s) from the owner(s) of each third-party copyrighted matter to be included in my work, allowing electronic distribution (if such use is not permitted by the fair use doctrine) which will be submitted to UKnowledge as Additional File. I hereby grant to The University of Kentucky and its agents the irrevocable, non-exclusive, and royalty-free license to archive and make accessible my work in whole or in part in all forms of media, now or hereafter known.
  • The Blunted Plasma Cortisol Response to Apomorphine and Its Relationship to Treatment Response in Patients with Schizophrenia Herbert Y

    The Blunted Plasma Cortisol Response to Apomorphine and Its Relationship to Treatment Response in Patients with Schizophrenia Herbert Y

    The Blunted Plasma Cortisol Response to Apomorphine and Its Relationship to Treatment Response in Patients with Schizophrenia Herbert Y. Meltzer, M.D., Myung A. Lee, M.D., and Karuna Jayathilake, M.S. The adrenocorticotropic hormone (ACTH) and cortisol compared to normal controls. Patients who responded to six responses to apomorphine (APO), a direct acting dopamine weeks of treatment with antipsychotic drugs had a higher (DA) agonist, have been reported to be significantly blunted cortisol response to APO compared to non-responders. The in neuroleptic-free patients with schizophrenia (SCH). This plasma GH, but not PRL, response to APO was blunted in study primarily examined the cortisol, but also the prolactin male patients with SCH. Neither plasma GH nor PRL (PRL) and growth hormone (GH), response to APO in responses to APO were related to treatment response at six patients with SCH compared to normal controls, as well as the weeks. These results provide further evidence of dopaminergic relationship between endocrine measures and response to dysfunction in SCH. Furthermore, the APO-stimulated antipsychotic drug treatment. APO, 0.01 mg/kg, or placebo cortisol response may be predictive of subsequent clinical was administered to 51–98 patients with SCH and 15–25 response to antipsychotic drug treatment. normal controls. Psychopathology was assessed at the baseline [Neuropsychopharmacology 24:278–290, 2001] and six weeks after drug treatment. The plasma cortisol © 2001 American College of Neuropsychopharmacology. response to APO was markedly blunted in patients with SCH Published by Elsevier Science Inc. KEY WORDS: Cortisol; Apomorphine; Antipsychotic drug; schizophrenia (SCH) in order to study the role of DA in Schizophrenia the etiology of schizophrenia and the mechanism of ac- tion of antipsychotic drugs (Meltzer et al.
  • Interaction of Pergolide with Central Dopaminergic Receptors (Parkinsonism/Adenylate Cyclase) MENEK GOLDSTEIN*, ABRAHAM LIEBERMAN*, Jow Y

    Interaction of Pergolide with Central Dopaminergic Receptors (Parkinsonism/Adenylate Cyclase) MENEK GOLDSTEIN*, ABRAHAM LIEBERMAN*, Jow Y

    Proc. Natl. Acad. Sci. USA Vol. 77, No. 6, pp. 3725-3728, June 1980 Neurobiology Interaction of pergolide with central dopaminergic receptors (parkinsonism/adenylate cyclase) MENEK GOLDSTEIN*, ABRAHAM LIEBERMAN*, Jow Y. LEW*, TAKU ASANO*, MYRNA R. ROSENFELDt, AND MAYNARD H. MAKMANt *New York University Medical Center, Departments of Psychiatry and Neurology, 560 First Avenue, New York, New York 10016; and tAlbert Einstein College of Medicine, Departments of Biochemistry and Molecular Pharmacology, Bronx, New York 10461 Communicated by Michael Heidelberger, February 12,1980 ABSTRACT The activity of pergolide, an N-propylergoline MATERIALS AND METHODS derivative, has been tested for stimulation of central dopa- minergic receptors. Binding to dopamine receptors shows that Materials. [3H]Dopamine (8.4 Ci/mmol), [3H]Spiroperidol pergolide acts as an agonist with respect to these receptors. GTP ([3H]Spi) (23 Ci/mmol), N-n-[3H]propylnorapomorphine decreases the potencies of dopamine agonists and of pergolide, ([3H]NPA) (75 Ci/nmol) were purchased from New England but not of bromocriptine, to displace [3HJspiroperidol {43HSpi) Nuclear (1 Ci = 3.7 X 1010 becquerels). Pergolide was a gift from striatal membrane sites. The GTP-sensitive site labeled from Eli Lilly, and bromocriptine from Sandoz Pharmaceu- by [3HJSpi seems to be localized on intrastriatal dopamine re- tical. ceptors. The potency of dopamine agonists and of pergolide to Binding Assay. Preparation of bovine or rat membranes and displace [3HJSpi from striatal receptor sites is reduced in membranes exposed to higher temperatures. Pergolide, but not the ensuing binding assay were carried out as described (13). hitherto-tested dopaminergic ergots, stimulates do amine- For routine assay each tube contained 1.8 ml.