Anipryl 30 mg (Canada)This page contains information on Anipryl 30 mg for veterinary use.
The information provided typically includes the following:
- Anipryl 30 mg Indications
- Warnings and cautions for Anipryl 30 mg
- Direction and dosage information for Anipryl 30 mg
Anipryl 30 mgThis treatment applies to the following species:
selegiline hydrochloride tablets U.S.P.
Anipryl 2 mg - DIN 02184508
Anipryl 5 mg - DIN 02184516
Anipryl 10 mg - DIN 02229982
Anipryl 15 mg - DIN 02184524
Anipryl 30 mg - DIN 02229983
PHARMACOLOGIC CLASSIFICATION: Monoamine oxidase Type B (MAO-B) inhibitor.
STRUCTURAL FORMULA AND CHEMISTRY: Selegiline hydrochloride is (R)-(-)-N, 2-proprinylphenylethylamine hydrochloride.
Molecular Formula: C13H17N HCl
Molecular Weight: 223.75
Anipryl (selegiline hydrochloride) 2 mg, 5 mg, 10 mg, 15 mg, and 30 mg tablets are almost white tablets containing 2, 5, 10, 15 or 30 mg of selegiline HCl.
ACTION: Anipryl has been shown to be effective treatment for pituitary dependent hyperadrenocorticism (PDH) in dogs as demonstrated by amelioration of clinical signs and improved regulation of the hypothalamic pituitary adrenal (HPA) axis. In each of three clinical trials there was a progressive improvement in endocrine function, as documented by results of low dose dexamethasone suppression (LDDS) tests.1,2 Significant clinical improvement was also demonstrated.1,2 Typical clinical signs of PDH include polydipsia, polyuria, increased frequency of urination and loss of housetraining, panting, reduced activity, changes in sleep patterns, altered appetite, obesity, alopecia, abdominal distention, reduced skin elasticity, thin skin, and poor hair growth.1-3 In clinical trials, dogs with PDH treated with Anipryl exhibited decreased body weight and improved body conformation determined by measurement, as well as amelioration of dermatologic signs (skin thickness and elasticity, alopecia, pyoderma) and regrowth of hair.1,2 Quality of life/general health was significantly improved based on increased behavioral and cognitive responses such as higher activity level, increased interaction with and responsiveness to the owner, decreased polydipsia and panting, improved housetraining habits and sleep patterns.1,2
The LDDS test is used to confirm dysregulation of the HPA axis, and to monitor endocrinologic response to therapy. Adrenocorticotropic hormone (ACTH) secretion from the pars intermedia of the canine pituitary gland, and corticotropin releasing hormone (CRH) mediated ACTH release from the pars distalis are tonically inhibited by central nervous system dopamine levels.5-7 Loss of this tonic inhibition results in increased secretion of ACTH, which results in adrenal hyperplasia and increased production of cortisol.7 Hypothalamic dopamine concentrations are decreased in dogs with PDH.8 Selegiline helps restore depleted central dopamine levels and facilitates dopaminergic transmission by several mechanisms, especially potent selective, irreversible inhibition of MAOB.1,9 Selegiline also increases the synthesis and release of dopamine into the synapse, and inhibits dopamine reuptake.9 Selegiline or its metabolites may enhance release of other neurotransmitters such as norepinephrine and serotonin.9
In the clinical trials noted above, dogs treated with Anipryl exhibited improvement in neuroendocrine function, as demonstrated by improvement (normalization in some patients) of LDDS test results.1,2 The precise mechanism for this continued improvement is unknown, but may involve neuroprotection or nerve rescue, in addition to the mechanisms noted above. Experiments in laboratory animals demonstrated that selegiline enhanced the survival of neurons after nerve trauma or exposure to neurotoxins.10,11
Canine PDH is a neuroendocrine disease which shares numerous features in common with several neurodegenerative disorders.2,12 For example, behavioral signs and cognitive impairment in subjects with HPA axis dysregulation may resemble some of the behavioral and cognitive impairments in people with Parkinson’s or Alzheimer’s disease.12,13 Clinical trials in people with these disorders have demonstrated that selegiline improves cognitive and other CNS functions.14,15 Studies in laboratory and pet dogs have also revealed age associated cognitive dysfunction which is responsive to selegiline therapy.12,16,17
Some neurodegenerative diseases, especially Parkinson’s disease, may represent abnormally rapid brain aging.18 Parkinsonian patients treated with selegiline lived longer than those not receiving the drug.19 Furthermore, laboratory animals treated with selegiline exhibited significantly longer life compared to placebo treated animals.20
Cognitive dysfunction is a clinical syndrome recognized by veterinarians and often described by pet owners as “senility,” “simple aging,” or “old dog syndrome.” The syndrome is typified by the presence of multiple cognitive impairments and behavioral problems which impair the dog’s function as a pet and cause the owner concern. Some of the typical signs include loss of housetraining; decreased interest in food; inactivity or inattention to environment, including people or other animals; confusion or disorientation; apparent inability to recognize familiar places, people or other animals; apparent inability to recognize/respond to commands or when called by name; apparent decrease in hearing; development of “compulsive” or repetitive behaviors or habits (some examples: pacing, “fly biting,” tail chasing, floor licking); wandering, or circling to BOTH sides (unilateral circling suggests a focal lesion); tremor or shaking; changes in sleep/wake patterns; or inappropriate vocalization.
Anipryl has been shown to be an effective treatment for cognitive dysfunction in dogs as demonstrated by amelioration of cognitive and behavioral signs and problems.1,12 After 1 month of Anipryl therapy, 75% of treated dogs exhibited cognitive improvement, and there were 78% and 77% improved at months 2 and 3, respectively. Efficacy was also evaluated for each individual parameter noted above. During the 3 months of Anipryl therapy, the population improved for all parameters at every time point, many of which attained statistical significance. Specifically, after 1 month of Anipryl therapy, the improvement reached significance or high significance for 13 (87%) of the 15 parameters; after months 2 and 3 of therapy the number of significantly improved parameters was 13 (87%) and 10 (67%), respectively.
TOXICITY: Selegiline hydrochloride was administered orally to beagle dogs once daily for one year at doses of 0, 1, 4 or 16 mg/kg. The no effect level was found to be 1 mg/kg. The following clinical signs were noted in some dogs at higher doses: salivation, panting, repetitive movements, decreased weight gain, and changes in activity level.
Anipryl 30 mg Indications
Cushing’s disease. Anipryl tablets are indicated for the treatment of uncomplicated pituitary dependent hyperadrenocorticism or Cushing’s disease in dogs. They are not indicated for other forms of Cushing’s syndrome.
Cognitive dysfunction. Anipryl tablets are indicated for the treatment of cognitive dysfunction syndrome in dogs.
PrecautionsEndocrine function testing to confirm pituitary dependent hyperadrenocorticism should be performed by a licensed veterinarian prior to initiation of therapy. If complications of PDH are evident at the time of diagnosis or emerge during Anipryl therapy the patient should be evaluated and, if warranted, alternative therapy considered. Concurrent use of Anipryl in conjunction with other therapy of canine PDH has not been reported. Anipryl should not be administered at doses exceeding those recommended.
REPRODUCTION: The effect of Anipryl on reproduction in the bitch has not been determined.
Anipryl is contraindicated in patients with known hypersensitivity to this drug. Controlled studies to determine the interaction of selegiline when administered with other drugs have not been conducted in dogs. To date, patients enrolled in clinical trials have not been reported to exhibit adverse drug interactions with heartworm prophylaxis, a variety of antimicrobials, anthelminthics and analgesics. Concurrent use of selegiline with other MAO inhibitors, such as Amitraz, is not recommended. In humans, selegiline is contraindicated for use with meperidine and this contraindication is often extended to other opioids. Further experience in humans has revealed adverse interactions between nonspecific MAO inhibitors and tricyclic antidepressants such as fluoxetine. Although to date no such interaction has been reported for selegiline in any nonhuman species, it seems prudent to avoid such combinations in dogs.
Side EffectsDuring clinical trials 156 dogs treated with Anipryl for as long as 2 years were monitored for the occurrence of adverse events. No serious adverse events thought to be related to Anipryl therapy were reported and no adverse drug interactions were reported.
Dosage and Administration
Cushing’s disease. After confirmation of the diagnosis of PDH, Anipryl is recommended orally once daily at an initial dose of 1 mg/kg of body weight. During the first two months of therapy, the patient should be reevaluated periodically for clinical response by history and physical examination. If no improvement in clinical signs or physical examination findings is evident by 2 months the dose can be increased to a maximum of 2 mg/kg once daily, and the dog reevaluated in similar fashion one month later. If there is still no improvement or if at any time clinical signs progress, the patient should be evaluated for the presence of concurrent disorders, including performance of appropriate laboratory tests or other studies as warranted. In dogs whose clinical signs of PDH progress despite Anipryl therapy in the absence of concurrent disease, alternative therapy should be considered.
Cognitive dysfunction. In dogs diagnosed with signs of cognitive dysfunction, Anipryl is recommended orally once daily at an initial dose of 0.5 mg/kg of body weight. Since many dogs with cognitive dysfunction are elderly, it is likely that concurrent medical problems unrelated to cognitive dysfunction will exist at the time of diagnosis of cognitive dysfunction, or emerge during therapy. Therefore, prior to, or concurrent with, initiation of Anipryl therapy, the patient should be evaluated for the presence of concurrent medical disorders, including performance of appropriate laboratory tests or other studies as warranted. Any medical problems present at the time of diagnosis should be treated and managed by the usual appropriate methods, while continuing Anipryl therapy. During the first two months of therapy, the patient should be reevaluated periodically for behavioral and clinical response by history and physical examination. If no improvement in behavioral response is evident by 2 months the dose can be increased to a maximum of 1 mg/kg once daily, and the dog reevaluated in similar fashion one month later. If there is no behavioral improvement or the behavioral signs progress, the patient should be evaluated for the presence of concurrent medical disorders, as directed above. Any medical problems identified should be treated and managed by usual, appropriate methods. In dogs whose behavioral signs progress despite Anipryl therapy when concurrent medical disorders have been controlled or eliminated, alternative therapy should be considered.
AVAILABILITY: Five tablet sizes are available in blister packages of 30’s: 2 mg, 5 mg, 10 mg, 15 mg and 30 mg.
StorageStore at or below 25°C.
1. Bureau of Veterinary Drugs, Health and Welfare Canada: Data on file.
2. Bruyette DS, Ruehl WW, Smidberg TL: Canine pituitary dependent hyperadrenocorticism: A spontaneous animal model for neurodegenerative disorders and their treatment with L-deprenyl. Progress in Brain Research (Yu PM, et al editors) 1995, Vol. 106; pp 207-215.
3. Feldman EC: Adrenal Gland Disease. Textbook of Veterinary Internal Medicine, 2nd Ed. (Ettinger SJ, ed). W.B. Saunders, Philadelphia, PA 1989, p 1721.
4. Rijnberk A, Mol JA, Kwant MM, et al: Effects of bromocriptine on corticotrophin, melanotrophin, and corticosteroid secretion in dogs with pituitary-dependent hyperadrenocorticism. J Endocrinol 118:271-277, 1988.
5. Kemppainen RJ, Zerbe CA, Sartin JL: Regulation and secretion of propiomelanocortin peptides from isolated perifused dog pituitary pars intermedia cells. Endocrinol 124:2208-2217, 1989.
6. Kemppainen RJ, Clark TP, Sartin JL, et al: Regulation of the adrenocorticotropin secretion from cultured canine anterior pituitary cells. Am J Vet Res 53:2355-2358, 1992.
7. Zerbe CA, Clark TP, Sartin JL, et al: Domperidone treatment enhances corticotropin-releasing hormone stimulated ACTH release from the dog pituitary. Neuroendocrinol 57:282-288, 1993.
8. Peterson ME, Palkovits M, Chiueh CC, et al: Biogenic amine and corticotropin-releasing factor concentrations in hypothalamic paraventricular nucleus and biogenic amine levels in the median eminence of normal dogs, chronic dexamethasone treated dogs, and dogs with naturally-occurring pituitary-dependent hyperadrenocorticism (canine Cushing’s disease). J Neuroendocrinol 1:169-171, 1989.
9. Heinonen EH, et al: A review of the pharmacology of selegiline. Acta Neurol Scand 84 (Suppl.) 136:44-59, 1991.
10. Tatton WG, Greenwood CE: Rescue of dying neurons: A new action for Deprenyl in MPTP parkinsonism. J Neurosci Res 30:666-672,1991.
11. Salo PT, Tatton WG: Deprenyl reduces the death of motoneurons caused by axotomy. J Neurosci Res 31:394-400, 1992.
12. Ruehl WW, et al: Canine cognitive dysfunction as a model for human age related cognitive decline, dementia and Alzheimer’s disease: Clinical presentation, cognitive testing, pathology and response to L-deprenyl therapy. Prog Brain Res (Yu PM, et al, eds) 1995, Vol 106, pp 217-225.
13. Lupien S, LeCours A, Lussier I, et al: Basal cortisol levels and cognitive deficits in human aging. J Neurosci 14:2893-2903, 1994.
14. Wessel K: MAOB inhibitors in neurological disorders with special reference to selegiline. Inhibitors of Monoamine Oxidase B (Szelenyi I, ed). Birkhauser Verlag, Basel, 1993; pp 253-275.
15. Tariot PN, Schneider LS, Patel SV, Goldstein B: Alzheimer’s disease and L-deprenyl: Rationales and findings. Inhibitors of Monoamine Oxidase B (Szelenyi I, ed). Birkhauser Verlag, Basel, 1993; pp 301-317.
16. Milgram NW, Ivy GO, Head E, et al: The effect of L-deprenyl on behavior, cognitive function, and biogenic amines in the dog. Neurochem Res 18:1211-1219, 1993.
17. Head E, Hartley J, Mehta R, et al: The effects of L-deprenyl on spatial short term memory in the dog (Abst). Soc Neurosci (Accepted for Publication).
18. Wolters ECh, Caine DB: Is Parkinson’s Disease related to aging? Parkinsonism and Aging (Caine DB, et al, eds). Raven Press, New York, 1987; pp 125-132.
19. Birkmayer W, Knoll J, Riederer P, et al: Increased life expectancy resulting from addition of L-deprenyl to madopar treatment in Parkinson’s Disease: A Long Term Study. J Neurol Transm 64:113-127, 1985.
20. Kitani K, Kanai S, et al: Chronic treatment of (-) deprenyl prolongs the life span of male fischer 344 rats. Further Evidence. Life Sci 52:281-288, 1993.
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