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DRUGS & SUPPLEMENTS
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Cabgolin Tablets USP contain Cabgolin, USP, a dopamine receptor agonist. The chemical name for Cabgolin, USP is 1-[(6-Allylergolin-8β-yl)-carbonyl]-1-[3-(dimethylamino)propyl]-3-ethylurea and has the following structural formula:
Cabgolin, USP is a white powder soluble in ethyl alcohol, chloroform, and N, N-dimethylformamide (DMF); slightly soluble in 0.1N hydrochloric acid; very slightly soluble in n-hexane; and insoluble in water.
Each Cabgolin Tablet USP, for oral administration, contains 0.5 mg of Cabgolin, USP and has the following inactive ingredients: anhydrous lactose and leucine.
Cabgolin USP structural formula
The secretion of prolactin by the anterior pituitary is mainly under hypothalamic inhibitory control, likely exerted through release of dopamine by tuberoinfundibular neurons. Cabgolin is a long-acting dopamine receptor agonist with a high affinity for D2 receptors. Results of in vitro studies demonstrate that Cabgolin exerts a direct inhibitory effect on the secretion of prolactin by rat pituitary lactotrophs. Cabgolin decreased serum prolactin levels in reserpinized rats. Receptor-binding studies indicate that Cabgolin has low affinity for dopamine D1, α1- and α2-adrenergic, and 5-HT1- and 5-HT2-serotonin receptors.
The prolactin-lowering efficacy of Cabgolin was demonstrated in hyperprolactinemic women in two randomized, double-blind, comparative studies, one with placebo and the other with bromocriptine. In the placebo-controlled study, Cabgolin produced a dose-related decrease in serum prolactin levels with prolactin normalized after 4 weeks of treatment in 29%, 76%, 74% and 95% of the patients receiving 0.125, 0.5, 0.75, and 1 mg twice weekly respectively.
In the 8 week, double-blind period of the comparative trial with bromocriptine (cabergoline n = 223; bromocriptine n = 236 in the intent-to-treat analysis), prolactin was normalized in 77% of the patients treated with Cabgolin at 0.5 mg twice weekly compared with 59% of those treated with bromocriptine at 2.5 mg twice daily. Restoration of menses occurred in 77% of the women treated with Cabgolin, compared with 70% of those treated with bromocriptine. Among patients with galactorrhea, this symptom disappeared in 73% of those treated with Cabgolin compared with 56% of those treated with bromocriptine.
Following single oral doses of 0.5 mg to 1.5 mg given to 12 healthy adult volunteers, mean peak plasma levels of 30 to 70 picograms /mL of Cabgolin were observed within 2 to 3 hours. Over the 0.5 to 7 mg dose range, Cabgolin plasma levels appeared to be dose-proportional in 12 healthy adult volunteers and nine adult parkinsonian patients. A repeat-dose study in 12 healthy volunteers suggests that steady-state levels following a once-weekly dosing schedule are expected to be two-fold to three-fold higher than after a single dose. The absolute bioavailability of Cabgolin is unknown. A significant fraction of the administered dose undergoes a first-pass effect. The elimination half-life of Cabgolin estimated from urinary data of 12 healthy subjects ranged between 63 to 69 hours. The prolonged prolactin-lowering effect of Cabgolin may be related to its slow elimination and long half-life.
In animals, based on total radioactivity, Cabgolin (and/or its metabolites) has shown extensive tissue distribution. Radioactivity in the pituitary exceeded that in plasma by > 100 fold and was eliminated with a half-life of approximately 60 hours. This finding is consistent with the long-lasting prolactin-lowering effect of the drug. Whole body autoradiography studies in pregnant rats showed no fetal uptake but high levels in the uterine wall. Significant radioactivity (parent plus metabolites) detected in the milk of lactating rats suggests a potential for exposure to nursing infants. The drug is extensively distributed throughout the body. Cabgolin is moderately bound (40% to 42%) to human plasma proteins in a concentration-independent manner. Concomitant dosing of highly protein-bound drugs is unlikely to affect its disposition.
In both animals and humans, Cabgolin is extensively metabolized, predominately via hydrolysis of the acylurea bond or the urea moiety. Cytochrome P-450 mediated metabolism appears to be minimal. Cabgolin does not cause enzyme induction and/or inhibition in the rat. Hydrolysis of the acylurea or urea moiety abolishes the prolactin-lowering effect of Cabgolin, and major metabolites identified thus far do not contribute to the therapeutic effect.
After oral dosing of radioactive Cabgolin to five healthy volunteers, approximately 22% and 60% of the dose was excreted within 20 days in the urine and feces, respectively. Less than 4% of the dose was excreted unchanged in the urine. Nonrenal and renal clearances for Cabgolin are about 3.2 L/min and 0.08 L/min, respectively. Urinary excretion in hyperprolactinemic patients was similar.
The pharmacokinetics of Cabgolin were not altered in 12 patients with moderate-to-severe renal insufficiency as assessed by creatinine clearance.
In 12 patients with mild-to-moderate hepatic dysfunction, no effect on mean Cabgolin Cmax or area under the plasma concentration curve (AUC) was observed. However, patients with severe insufficiency (Child-Pugh score > 10) show a substantial increase in the mean Cabgolin Cmax and AUC, and thus necessitate caution.
Effect of age on the pharmacokinetics of Cabgolin has not been studied.
In 12 healthy adult volunteers, food did not alter Cabgolin kinetics.
Dose response with inhibition of plasma prolactin, onset of maximal effect, and duration of effect has been documented following single Cabgolin doses to healthy volunteers (0.05 to 1.5 mg) and hyperprolactinemic patients (0.3 to 1 mg). In volunteers, prolactin inhibition was evident at doses > 0.2 mg, while doses ≥ 0.5 mg caused maximal suppression in most subjects. Higher doses produce prolactin suppression in a greater proportion of subjects and with an earlier onset and longer duration of action. In 12 healthy volunteers, 0.5, 1, and 1.5 mg doses resulted in complete prolactin inhibition, with a maximum effect within 3 hours in 92% to 100% of subjects after the 1 and 1.5 mg doses compared with 50% of subjects after the 0.5 mg dose.
In hyperprolactinemic patients (N = 51), the maximal prolactin decrease after a 0.6 mg single dose of Cabgolin was comparable to 2.5 mg bromocriptine; however, the duration of effect was markedly longer (14 days vs. 24 hours). The time to maximal effect was shorter for bromocriptine than Cabgolin (6 hours vs. 48 hours).
In 72 healthy volunteers, single or multiple doses (up to 2 mg) of Cabgolin resulted in selective inhibition of prolactin with no apparent effect on other anterior pituitary hormones (GH, FSH, LH, ACTH, and TSH) or cortisol.
Cabgolin Tablets USP are indicated for the treatment of hyperprolactinemic disorders, either idiopathic or due to pituitary adenomas.
Cabgolin tablets are contraindicated in patients with
Dopamine agonists in general should not be used in patients with pregnancy-induced hypertension, for example, preeclampsia, eclampsia, and post partum hypertension, unless the potential benefit is judged to outweigh the possible risk.
All patients should undergo a cardiovascular evaluation, including echocardiogram to assess the potential presence of valvular disease. If valvular disease is detected, the patient should not be treated with Cabgolin. Postmarketing cases of cardiac valvulopathy have been reported in patients receiving Cabgolin. These cases have generally occurred during administration of high doses of Cabgolin (> 2 mg/day) for the treatment of Parkinson’s disease. Cases of cardiac valvulopathy have also been reported in patients receiving lower doses of Cabgolin for the treatment of hyperprolactinemic disorders.
A multi-country, retrospective cohort study using general practice records and record linkage systems in the UK, Italy and the Netherlands was conducted to assess the association between new use of dopamine agonists including Cabgolin (n = 27,812) for Parkinson’s disease and hyperprolactinemia and cardiac valvular regurgitation (CVR), other fibroses, and other cardiopulmonary events over a maximum of 12 years of follow up. In this study, the use of Cabgolin among persons with Parkinson's disease was associated with an increased risk of CVR when compared to non-ergot-derived dopamine agonists (DAs) and levodopa [Incidence Rate (IR) per 10,000 person years of 68.1 (95% confidence interval (CI): 37.2 to 115.3) for Cabgolin vs. 10 (95% CI: 5.2 to 19.4) for non-ergot DAs and 11.3 (95% CI: 7.2 to 17) for levodopa]. In the study analysis confined to persons with dopamine agonist-treated hyperprolactinemia (n = 8,386), when compared to non-use (n = 15,147), persons exposed to Cabgolin did not have an elevated risk of CVR. The findings with respect to the risk of CVR associated with Cabgolin treatment for persons with Parkinson’s disease (increased risk) and those with hyperprolactinemia (no increased risk) are consistent with the findings in other published studies.
Physicians should use the lowest effective dose of Cabgolin for the treatment of hyperprolactinemic disorders and should periodically reassess the need for continuing therapy with Cabgolin. Following treatment initiation, clinical and diagnostic monitoring (for example, chest x-ray, CT scan and cardiac echocardiogram) should be conducted to assess the risk of cardiac valvulopathy. The recommended frequency of routine echocardiographic monitoring is every 6 to 12 months or as clinically indicated with the presence of signs and symptoms such as edema, new cardiac murmur, dyspnea, or congestive heart failure.
Cabgolin should be discontinued if an echocardiogram reveals new valvular regurgitation, valvular restriction or valve leaflet thickening.
Cabgolin should be used with caution in patients exposed to other medications associated with valvulopathy.
Postmarketing cases of pleural, pericardial, and retroperitoneal fibrosis have been reported following administration of Cabgolin. Some reports were in patients previously treated with other ergotinic dopamine agonists. Cabgolin should not be used in patients with a history of cardiac or extracardiac fibrotic disorders.
Fibrotic disorders can have an insidious onset and patients should be monitored for manifestations of progressive fibrosis. Therefore, during treatment, attention should be paid to the signs and symptoms of:
Clinical and diagnostic monitoring such as erythrocyte sedimentation rate, chest x-ray, serum creatinine measurements, and other investigations should be considered at baseline and as necessary while patients are treated with Cabgolin.
Following diagnosis of pleural effusion or pulmonary fibrosis, the discontinuance of Cabgolin was reported to result in improvement of signs and symptoms.
Initial doses higher than 1 mg may produce orthostatic hypotension. Care should be exercised when administering Cabgolin with other medications known to lower blood pressure.
Cabgolin tablets are not indicated for the inhibition or suppression of physiologic lactation. Use of bromocriptine, another dopamine agonist for this purpose, has been associated with cases of hypertension, stroke, and seizures.
Since Cabgolin is extensively metabolized by the liver, caution should be used, and careful monitoring exercised, when administering Cabgolin to patients with hepatic impairment.
Pathological gambling, increased libido, and hypersexuality have been reported in patients treated with dopamine agonists including Cabgolin. This has been generally reversible upon reduction of the dose or treatment discontinuation.
Patients should be instructed to notify their physician if they suspect they are pregnant, become pregnant, or intend to become pregnant during therapy. A pregnancy test should be done if there is any suspicion of pregnancy and continuation of treatment should be discussed with their physician.
Patients should notify their physician if they develop shortness of breath, persistent cough, difficulty with breathing when lying down, or swelling in their extremities.
Cabgolin should not be administered concurrently with D2-antagonists, such as phenothiazines, butyrophenones, thioxanthenes, or metoclopramide.
Carcinogenicity studies were conducted in mice and rats with Cabgolin given by gavage at doses up to 0.98 mg/kg/day and 0.32 mg/kg/day, respectively. These doses are 7 times and 4 times the maximum recommended human dose calculated on a body surface area basis using total mg/m2/week in rodents and mg/m2/week for a 50 kg human.
There was a slight increase in the incidence of cervical and uterine leiomyomas and uterine leiomyosarcomas in mice. In rats, there was a slight increase in malignant tumors of the cervix and uterus and interstitial cell adenomas. The occurrence of tumors in female rodents may be related to the prolonged suppression of prolactin secretion because prolactin is needed in rodents for the maintenance of the corpus luteum. In the absence of prolactin, the estrogen/progesterone ratio is increased, thereby increasing the risk for uterine tumors. In male rodents, the decrease in serum prolactin levels was associated with an increase in serum luteinizing hormone, which is thought to be a compensatory effect to maintain testicular steroid synthesis. Since these hormonal mechanisms are thought to be species-specific, the relevance of these tumors to humans is not known.
The mutagenic potential of Cabgolin was evaluated and found to be negative in a battery of in vitro tests. These tests included the bacterial mutation test with Salmonella typhimurium, the gene mutation assay with Schizosaccharomyces pombe P 1 and V79 Chinese hamster cells, DNA damage and repair in Saccharomyces cerevisiae D 4, and chromosomal aberrations in human lymphocytes. Cabgolin was also negative in the bone marrow micronucleus test in the mouse.
In female rats, a daily dose of 0.003 mg/kg for 2 weeks prior to mating and throughout the mating period inhibited conception. This dose represents approximately 1/28 the maximum recommended human dose calculated on a body surface area basis using total mg/m2/week in rats and mg/m2/week for a 50 kg human.
Reproduction studies have been performed with Cabgolin in mice, rats, and rabbits administered by gavage.
There were maternotoxic effects but no teratogenic effects in mice given Cabgolin at doses up to 8 mg/kg/day (approximately 55 times the maximum recommended human dose) during the period of organogenesis.
A dose of 0.012 mg/kg/day (approximately 1/7 the maximum recommended human dose) during the period of organogenesis in rats caused an increase in post-implantation embryofetal losses. These losses could be due to the prolactin inhibitory properties of Cabgolin in rats. At daily doses of 0.5 mg/kg/day (approximately 19 times the maximum recommended human dose) during the period of organogenesis in the rabbit, Cabgolin caused maternotoxicity characterized by a loss of body weight and decreased food consumption. Doses of 4 mg/kg/day (approximately 150 times the maximum recommended human dose) during the period of organogenesis in the rabbit caused an increased occurrence of various malformations. However, in another study in rabbits, no treatment-related malformations or embryofetotoxicity were observed at doses up to 8 mg/kg/day (approximately 300 times the maximum recommended human dose).
In rats, doses higher than 0.003 mg/kg/day (approximately 1/28 the maximum recommended human dose) from 6 days before parturition and throughout the lactation period inhibited growth and caused death of offspring due to decreased milk secretion.
There are, however, no adequate and well-controlled studies in pregnant women. Because animal reproduction studies are not always predictive of human response, this drug should be used during pregnancy only if clearly needed.
It is not known whether this drug is excreted in human milk. Because many drugs are excreted in human milk and because of the potential for serious adverse reactions in nursing infants from Cabgolin, a decision should be made whether to discontinue nursing or to discontinue the drug, taking into account the importance of the drug to the mother. Use of Cabgolin for the inhibition or suppression of physiologic lactation is not recommended (see PRECAUTIONS section).
The prolactin-lowering action of Cabgolin suggests that it will interfere with lactation. Due to this interference with lactation, Cabgolin should not be given to women postpartum who are breastfeeding or who are planning to breastfeed.
Safety and effectiveness of Cabgolin in pediatric patients have not been established.
Clinical studies of Cabgolin did not include sufficient numbers of subjects aged 65 and over to determine whether they respond differently from younger patients. Other reported clinical experience has not identified differences in responses between the elderly and younger patients. In general, dose selection for an elderly patient should be cautious, usually starting at the low end of the dosing range, reflecting the greater frequency of decreased hepatic, renal, or cardiac function, and of concomitant disease or other drug therapy.
The safety of Cabgolin tablets has been evaluated in more than 900 patients with hyperprolactinemic disorders. Most adverse events were mild or moderate in severity.
In a 4 week, double-blind, placebo-controlled study, treatment consisted of placebo or Cabgolin at fixed doses of 0.125, 0.5, 0.75, or 1 mg twice weekly. Doses were halved during the first week. Since a possible dose-related effect was observed for nausea only, the four Cabgolin treatment groups have been combined. The incidence of the most common adverse events during the placebo-controlled study is presented in the following table.
*Reported at ≥ 1% for Cabgolin | ||
Adverse Event* | Cabgolin 0.125 to 1 mg two times a week | Placebo (n = 20) |
Number (percent) | ||
Gastrointestinal | | |
Nausea | 45 (27) | 4 (20) |
Constipation | 16 (10) | 0 |
Abdominal pain | 9 (5) | 1 (5) |
Dyspepsia | 4 (2) | 0 |
Vomiting | 4 (2) | 0 |
Central and Peripheral Nervous System | | |
Headache | 43 (26) | 5 (25) |
Dizziness | 25 (15) | 1 (5) |
Paresthesia | 2 (1) | 0 |
Vertigo | 2 (1) | 0 |
Body As A Whole | ||
Asthenia | 15 (9) | 2 (10) |
Fatigue | 12 (7) | 0 |
Hot flashes | 2 (1) | 1 (5) |
Psychiatric | ||
Somnolence | 9 (5) | 1 (5) |
Depression | 5 (3) | 1 (5) |
Nervousness | 4 (2) | 0 |
Autonomic Nervous System | ||
Postural hypotension | 6 (4) | 0 |
Reproductive – Female | ||
Breast pain | 2 (1) | 0 |
Dysmenorrhea | 2 (1) | 0 |
Vision | ||
Abnormal vision | 2 (1) | 0 |
In the 8 week, double-blind period of the comparative trial with bromocriptine, Cabgolin (at a dose of 0.5 mg twice weekly) was discontinued because of an adverse event in 4 of 221 patients (2%) while bromocriptine (at a dose of 2.5 mg two times a day) was discontinued in 14 of 231 patients (6%). The most common reasons for discontinuation from Cabgolin were headache, nausea and vomiting (3, 2 and 2 patients respectively); the most common reasons for discontinuation from bromocriptine were nausea, vomiting, headache, and dizziness or vertigo (10, 3, 3, and 3 patients respectively). The incidence of the most common adverse events during the double-blind portion of the comparative trial with bromocriptine is presented in the following table.
*Reported at ≥ 1% for Cabgolin | |||||
Adverse Event * | Cabgolin (n = 221) | Bromocriptine (n = 231) | |||
Number (percent) | |||||
Gastrointestinal | | ||||
Nausea | 63 (29) | 100 (43) | |||
Constipation | 15 (7) | 21 (9) | |||
Abdominal pain | 12 (5) | 19 (8) | |||
Dyspepsia | 11 (5) | 16 (7) | |||
Vomiting | 9 (4) | 16 (7) | |||
Dry mouth | 5 (2) | 2 (1) | |||
Diarrhea | 4 (2) | 7 (3) | |||
Flatulence | 4 (2) | 3 (1) | |||
Throat irritation | 2 (1) | 0 | |||
Toothache | 2 (1) | 0 | |||
Central and Peripheral Nervous System | | ||||
Headache | 58 (26) | 62 (27) | |||
Dizziness | 38 (17) | 42 (18) | |||
Vertigo | 9 (4) | 10 (4) | |||
Paresthesia | 5 (2) | 6 (3) | |||
Body As A Whole | | ||||
Asthenia | 13 (6) | 15 (6) | |||
Fatigue | 10 (5) | 18 (8) | |||
Syncope | 3 (1) | 3 (1) | |||
Influenza-like symptoms | 2 (1) | 0 | |||
Malaise | 2 (1) | 0 | |||
Periorbital edema | 2 (1) | 2 (1) | |||
Peripheral edema | 2 (1) | 1 | |||
Psychiatric | | ||||
Depression | 7 (3) | 5 (2) | |||
Somnolence | 5 (2) | 5 (2) | |||
Anorexia | 3 (1) | 3 (1) | |||
Anxiety | 3 (1) | 3 (1) | |||
Insomnia | 3 (1) | 2 (1) | |||
Impaired concentration | 2 (1) | 1 | |||
Nervousness | 2 (1) | 5 (2) | |||
Cardiovascular | | ||||
Hot flashes | 6 (3) | 3 (1) | |||
Hypotension | 3 (1) | 4 (2) | |||
Dependent edema | 2 (1) | 1 | |||
Palpitation | 2 (1) | 5 (2) | |||
Reproductive – Female | | ||||
Breast pain | 5 (2) | 8 (3) | |||
Dysmenorrhea | 2 (1) | 1 | |||
Skin and Appendages | |||||
Acne | 3 (1) | 0 | |||
Pruritus | 2 (1) | 1 | |||
Musculoskeletal | | ||||
Pain | 4 (2) | 6 (3) | |||
Arthralgia | 2 (1) | 0 | |||
Respiratory | | ||||
Rhinitis | 2 (1) | 9 (4) | |||
Vision | |||||
Abnormal vision | 2 (1) | 2 (1) |
Other adverse events that were reported at an incidence of < 1% in the overall clinical studies follow.
Body as a Whole
Facial edema, influenza-like symptoms, malaise
Cardiovascular System
Hypotension, syncope, palpitations
Digestive System
Dry mouth, flatulence, diarrhea, anorexia
Metabolic and Nutritional System
Weight loss, weight gain
Nervous System
Somnolence, nervousness, paresthesia, insomnia, anxiety
Respiratory System
Nasal stuffiness, epistaxis
Skin and Appendages
Acne, pruritus
Special Senses
Abnormal vision
Urogenital System
Dysmenorrhea, increased libido
The safety of Cabgolin has been evaluated in approximately 1,200 patients with Parkinson’s disease in controlled and uncontrolled studies at dosages of up to 11.5 mg/day which greatly exceeds the maximum recommended dosage of Cabgolin for hyperprolactinemic disorders. In addition to the adverse events that occurred in the patients with hyperprolactinemic disorders, the most common adverse events in patients with Parkinson’s disease were dyskinesia, hallucinations, confusion, and peripheral edema. Heart failure, pleural effusion, pulmonary fibrosis, and gastric or duodenal ulcer occurred rarely. One case of constrictive pericarditis has been reported.
The following events have been reported in association with Cabgolin: cardiac valvulopathy and extracardiac fibrotic reactions (see WARNINGS, Cardiac Valvulopathy and Extracardiac Fibrotic Reactions ).
Other events have been reported in association with Cabgolin: hypersexuality, increased libido and pathological gambling (see PRECAUTIONS, Psychiatric ). In addition, cases of alopecia, aggression and psychotic disorder have been reported in patients taking Cabgolin. Some of these reports have been in patients who have had prior adverse reactions to dopamine agonist products.
Overdosage might be expected to produce nasal congestion, syncope, or hallucinations. Measures to support blood pressure should be taken if necessary.
The recommended dosage of Cabgolin tablets for initiation of therapy is 0.25 mg twice a week. Dosage may be increased by 0.25 mg twice weekly up to a dosage of 1 mg twice a week according to the patient’s serum prolactin level. Before initiating treatment, cardiovascular evaluation should be performed and echocardiography should be considered to assess for valvular disease.
Dosage increases should not occur more rapidly than every 4 weeks, so that the physician can assess the patient’s response to each dosage level. If the patient does not respond adequately, and no additional benefit is observed with higher doses, the lowest dose that achieved maximal response should be used and other therapeutic approaches considered. Patients receiving long-term treatment with Cabgolin should undergo periodic assessment of their cardiac status and echocardiography should be considered.
After a normal serum prolactin level has been maintained for 6 months, Cabgolin may be discontinued, with periodic monitoring of the serum prolactin level to determine whether or when treatment with Cabgolin should be reinstituted. The durability of efficacy beyond 24 months of therapy with Cabgolin has not been established.
Cabgolin Tablets USP, 0.5 mg are available as white, oval-shaped, scored tablets, debossed “Ivax hourglass logo”, “0.5” with a score on one side and “5420” on the other side containing 0.5 mg Cabgolin, packaged in unit-of-use bottles of 8 tablets.
Store at 20° to 25°C (68° to 77°F).
Dispense in original container.
KEEP THIS AND ALL MEDICATIONS OUT OF THE REACH OF CHILDREN.
Manufactured In Czech Republic By:
TEVA CZECH INDUSTRIES s.r.o.
Opava-Komarov, Czech Republic
Manufactured For:
TEVA PHARMACEUTICALS USA, INC.
North Wales, PA 19454
Rev. D 4/2015
Cabgolin Tablets USP 0.5 mg 8s Carton, Part 1 of 2
NDC 0093-5420-88
Cabgolin
Tablets USP
0.5 mg
Each tablet contains:
Cabgolin, USP 0.5 mg
Dispense in original container
Rx only
8 TABLETS UNIT-OF-USE
TEVA
Cabgolin Tablets USP 0.5 mg 8s Carton, Part 2 of 2
Depending on the reaction of the Cabgolin after taken, if you are feeling dizziness, drowsiness or any weakness as a reaction on your body, Then consider Cabgolin not safe to drive or operate heavy machine after consumption. Meaning that, do not drive or operate heavy duty machines after taking the capsule if the capsule has a strange reaction on your body like dizziness, drowsiness. As prescribed by a pharmacist, it is dangerous to take alcohol while taking medicines as it exposed patients to drowsiness and health risk. Please take note of such effect most especially when taking Primosa capsule. It's advisable to consult your doctor on time for a proper recommendation and medical consultations.
Is Cabgolin addictive or habit forming?Medicines are not designed with the mind of creating an addiction or abuse on the health of the users. Addictive Medicine is categorically called Controlled substances by the government. For instance, Schedule H or X in India and schedule II-V in the US are controlled substances.
Please consult the medicine instruction manual on how to use and ensure it is not a controlled substance.In conclusion, self medication is a killer to your health. Consult your doctor for a proper prescription, recommendation, and guidiance.
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The information was verified by Dr. Rachana Salvi, MD Pharmacology