Regapen qanday dori

Pulmonary oedema, throat tightness

Regapen qanday dori

Sog’ligingizga ziyon yetkazmang .
Saytda ko’rsatilgan ma’lumotlardan faqat mutaxassis provizor yoki shifokor bilan maslaxatlashgandan so’ng foydalaning.

Preparat haqida asosiy ma’lumotlar

Tarkibi:

1 kapsula quyidagilarni saqlaydi: faol modda: pregabalin 150 mg, 300 mg, yordamchi moddalar: laktoza monogidrati, prejelatinlangan makkajo‘xori kraxmali, talk.

Ta’sir etuvchi modda(XPN):

Preparatning savdo nomi:

Farmakalogik guruhi:

tutqanoqqa qarshi preparat.

Dori shakli:

qattiq jelatinli, oq tiniq bo‘lmagan kapsulalar.
Farmakoterapevtik guruhi
tutqanoqqa qarshi preparat.
Farmakokinetikasi

Tavsiya qilingan sutkalik dozalar diapozonida pregabalinning farmakokinetikasi bir tekis xarakterga ega bo‘lib, shaxslararo o‘zgaruvchanligi past (

Qo’llanilishi

Neyropatik og‘riq: kattalarda neyropatik og‘riqni davolash. Tutqanoq: ikkilamchi tarqalish bilan yoki usiz kechuvchi partsial tirishishlari bo‘lgan kattalarda yordamchi davolash vositasi sifatida. Tarqoq xavotirli buzilishlar kattalarda tarqoq xavotirli buzilishlarni davolash. Fibromialgiya: kattalarda fibromialgiyani davolash uchun qo‘llanadi.

Qo’llash usuli va do’zalari

Preparat ichga, ovqat qabul qilishdan qat’iy nazar, 150 dan 600 mg gacha bo‘lgan sutkalik dozada 2 yoki 3 martada qabul qilinadi. Neyropatik og‘riqda davolashni sutkada 150 mg dozadan boshlanadi. Erishilgan samarani va preparatni o‘zlashtira olinishini hisobga olib, 3-7 kundan keyin dozani sutkada 300 mg gacha, zarurati bo‘lganida yana 7 kundan keyin – maksimal doza sutkada 600 mg gacha oshirish mumkin. Tutqanoqda davolashni sutkada 150 mg dozadan boshlanadi. Erishilgan samarani va preparatni o‘zlashtira olinishini hisobga olib, 1 haftadan keyin dozani sutkada 300 mg gacha, yana 1 haftadan keyin – maksimal doza sutkada 600 mg gacha oshirish mumkin. Fibromialgiyada davolashni sutkada 2 marta 75 mg dozadan (sutkada 150 mg dozadan) boshlanadi. Erishilgan samarani va preparatni o‘zlashtira olinishini hisobga olib, 3-7 kundan keyin dozani sutkada 300 mg gacha oshirish mumkin. Ijobiy samara bo‘lmaganida dozani sutkada 450 mg gacha, zarurati bo‘lganida yana 7 kundan keyin – maksimal doza sutkada 600 mg gacha oshiriladi. Tarqoq xavotirli buzilishlarda davolashni sutkada 150 mg dozadan boshlanadi. Erishilgan samarani va preparatni o‘zlashtira olinishini hisobga olib, 7 kundan keyin dozani sutkada 300 mg gacha oshirish mumkin. Ijobiy samara bo‘lmaganida dozani sutkada 450 mg gacha, zarurati bo‘lganida yana 7 kundan keyin – maksimal doza sutkada 600 mg gacha oshiriladi. Regapen preparatini bekor qilish: agar davolashni to‘xtatish zarurati bo‘lsa, unda buni asta-sekin kamida 1 hafta davomida amalga oshirish tavsiya qilinadi. Buyrak faoliyatini buzilishi bo‘lgan patsiyentlarda doza shaxsiy ravishda KK bog‘liq holda tanlanadi (1-jadval), u quyidagi formula bo‘yicha hisoblanadi. Erkaklar uchun: KK (ml/min) = (tana vazni kg larda) x (140 – yosh (yillar hisobida)) /72 x zardob kreatinini (mg/dl). Ayollar uchun: KK (ml/min) = erkaklar uchun KK ko‘rsatkichi x 0,85. Gemodializda davolanayotgan patsiyentlarda pregabalinning sutkalik dozasi buyrak faoliyatiga bog‘liq holda tanlanadi. Bevosita har 4 soatlik gemodializ seansidan keyin qo‘shimcha doza buyuriladi (jadval).

Nojo’ya ta’sirlar

Pregabalinni klinik qo‘llanishi bo‘yicha mavjud bo‘lgan tajriba bo‘yicha 12000 dan ko‘proq patsiyentlarda eng tarqalgan nojo‘ya holatlar bosh aylanishi va uyquchanlik bo‘lgan. Kuzatiladigan holatlar odatda yengil yoki o‘rtacha darajada bo‘lgan. Pregabalin va platseboni nojo‘ya reaktsiyalari tufayli bekor qilish tez-tezligi muvofiq ravishda 14 va 7% ni tashkil qilgan. Davolashni to‘xtatilishini talab qiluvchi asosiy nojo‘ya samaralari ularni subyektiv o‘zlashtiraolishligiga qarab, bosh aylanishi (4%) va uyquchanlik (3%) bo‘lgan. Preparatni bekor qilinishiga olib kelgan yana boshqa nojo‘ya samaralar: ataksiya, ongni chalkashishi, asteniya, diqqatni buzilishi, ko‘rishni noaniqligi, koordinatsiyani buzilishi, periferik shishlar. Jadvalda barcha nojo‘ya holatlar sanab o‘tilgan, ularning tez-tezligi platsebo guruhidagidan ortiq bo‘lgan (1 odamdan ko‘pida kuzatiladigan) va asosiy kasallik va/yoki yo‘ldosh davolash bilan bog‘liq bo‘lishi mumkin bo‘lgan. Nojo‘ya reapktsiyalarning tez-tezligi tasnifi: juda tez-tez (>1/10), tez-tez (>1/100, 1/1000,

Qo’llash mumkin bo`lmagan holatlar

Bolalar va 17 yoshgacha bo‘lgan o‘smirlar (qo‘llash bo‘yicha ma’lumotlar yo‘q);Kam uchraydigan nasliy kasalliklar, shu jumladan galaktozani o‘zlashtiraolmaslik, laktaza yetishmovchiligi va glyukoza/galaktozani so‘rilishini buzilishi;preparatning komponentlariga yuqori sezuvchanlikda qo‘llash mumkin emas. Preparatni buyrak yetishmovchiligida, yurak yetishmovchiligida ehtiyotkorlik bilan buyurish kerak. Pregabalinni nazoratsiz qo‘llashning yakka hollari qayd etilganligi tufayli, uni anamnezida doriga qaramlik bo‘lgan patsiyentlarda ehtiyotkorlik bilan buyurish lozim (bunday patsiyentlar preparat bilan davolanish vaqtida sinchkov tibbiy kuzatuvga muhtojdirlar).

Dorilarning o’zaro ta’siri

Pregabalin asosan o‘zgarmagan holda siydik bilan chiqariladi, odamda minimal metabolizmga uchraydi (metabolitlar ko‘rinishida siydik bilan dozaning 2% dan kami chiqariladi), in vitro sharoitida boshqa dori vositalarining metabolizmini ingibirlamaydi va plazma oqsillari bilan bog‘lanmaydi, shuning uchun u farmakokinetik o‘zaro ta’sirga kirishish qobiliyatiga ega emas. Pregabalinni fenitoin, karbamazepin, valproat kislotasi, lamotridjin, gabapentin, lorazepam, oksikodon va etanol bilan klinik ahamiyatli darajadagi farmakokinetik o‘zaro ta’sirining belgilari aniqlanmagan. Peroral gipoglikemik preparatlar, diuretiklar, insulin, fenobarbital, tiagabin va topiramatni pregabalinning klirensiga klinik ahamiyatli daraja ta’sir ko‘rsatmasligi aniqlangan. Noretisteron va/yoki etinilestradiol saqlovchi peroral kontratseptivlar pregabalin bilan bir vaqtda qo‘llanganida ikkala preparatning muvozanatli farmakokinetikasi o‘zgarmagan. Pregabalinni va markaziy nerv tizimini susaytiruvchi boshqa preparatlarni bir vaqtda qo‘llanganda nafasni buzilishi va komani rivojlanish holatlari to‘g‘risida xabar berilgan. Shuningdek qabziyatni chaqiruvchi dori vositalar (masalan, opioid analgetiklar) bilan bir vaqtda qo‘llanganida me’da-ichak yo‘llarining faoliyatiga pregabalinning salbiy ta’siri (shu jumladan ichakni tutilishi, paralitik ileus, qabziyatni rivojlanishi) to‘g‘risida xabar berilgan. Pregabalinni oksikodon, lorazepam yoki etanol bilan takroran peroral qo‘llanilishi nafas olishga klinik ahamiyatli darajada ta’sir ko‘rsatmagan. Pregabalin, ehtimol oksikadon chaqirgan kognitiv va harakat buzilishlarini kuchaytirsa kerak. Pregabalin etanol va lorazepamning samaralarini kuchaytirishi mumkin.

Maxsus ko’rsatmalar

Qandli diabeti bo‘lgan ayrim bemorlarda pregabalin bilan davolash fonida tana vaznini oshishi hollarida, gipoglikemik preparatlarning dozasini to‘g‘rilash talab qilinishi mumkin. Angionevrotik shish simptomlari (masalan, yuzni shishi, perioral shish yoki yuqori nafas yo‘llarini shishi) rivojlangan hollarda pregabalinni bekor qilish lozim. Tutqanoqqa qarshi preparatlar, shu jumladan pregabalin suitsidal fikr yoki xatti-harakatlarni paydo bo‘lish xavfini oshirishi mumkin. Shuning uchun bu preparatlarni qabul qilayotgan patsiyentlarni depressiyani yuz berishi yoki og‘irlashishi, suitsidal fikr yoki xatti-harakatlarni paydo bo‘lishi yuzasidan sinchkovlik bilan kuzatish kerak. Pregabalin bilan davolash bosh aylanishi va uyquchanlik bilan kechgan, ular keksa odamlarda tasodifiy jarohatlar (yiqilish) xavfini oshiradi. Preparatni postmarketing qo‘llanishi davrida shuningdek hushdan ketish, ongni chalkashishi va kognitiv faoliyatni buzilishlari kabi holatlar aniqlangan. Shuning uchun bemorlar preparatning bo‘lishi mumkin bo‘lgan samaralarini baholab bo‘lmagunicha, ehtiyotkorlikka rioya qilishlari kerak. Pregabalin bilan tirishishlar bostirilganida boshqa tirishishga qarshi vositalarni bekor qilish mumkinligi va bu preparat bilan monodavolash maqsadga muvofiqligi to‘g‘risidagi ma’lumotlar yetarli emas. Pregabalinni qo‘llash fonida yoki davolash tugaganidan keyin o‘sha zahoti tirishishlar, shu jumladan tutqanoq holati va kichik xurujlarni rivojlanishi to‘g‘risida xabarlar bor. Pregabalin bilan davolanish vaqtida ko‘rishni noaniqligi yoki ko‘rish a’zolari tomonidan boshqa buzilishlar kabi nohush reaktsiyalar paydo bo‘lganida, preparatni bekor qilish ko‘rsatilgan simptomlarni yo‘qolishiga olib kelishi mumkin. Shuningdek buyrak yetishmovchiligini rivojlanish hollari aniqlangan, ayrim hollarda pregabalin bekor qilinganidan keyin buyrak faoliyati tiklangan. Pregabalin bilan davolashning qisqa yoki uzoq muddatlari tugaganidan keyin quyidagi uyqusizlik, bosh og‘rig‘i, ko‘ngil aynishi, diareya, grippsimon sindrom, depressiya, kuchli terlash, bosh aylanishi, tirishishlar va xavotirlik kabi nohush holatlar kuzatilgan. Pregabalinni bekor qilish sindromini ko‘rinishlarini tezligi va yaqqolligini, preparat bilan davolash davomiyligi va uning dozasi bilan bog‘liqligi to‘g‘risida ma’lumotlar mavjud emas. Preparatni postmarketing qo‘llash vaqtida ayrim patsiyentlarda pregabalin bilan davolash fonida surunkali yurak yetishmovchiligini rivojlanishi to‘g‘risida xabar berilgan. Bu reaktsiyalar asosan yurak faoliyatini buzilishlari bo‘lgan keksa yoshdagi va preparatni nevropatiya yuzasidan qabul qilgan bemorlarda kuzatilgan. Shuning uchun pregabalinni ushbu toifa patsiyentlarda ehtiyotkorlik bilan qo‘llash kerak. Pregabalin bekor qilinganidan keyin bunga o‘xshash reaktsiyalarning ko‘rinishlari yo‘qolishi mumkin. Markaziy nerv tizimi tomonidan, ayniqsa uyquchanlik kabi nohush holatlarning tez-tezligi, orqa miyani shikastlanishi bilan bog‘liq bo‘lgan markaziy neyropatik og‘riqni davolashda oshadi, ammo bu pregabalin va boshqa parallel qabul qilinayotgan vositalar (masalan, antispastik vositalar) ning samaralarni yig‘indisi oqibatida yuz berishi mumkin. Bu holatni pregabalinni ushbu ko‘rsatma yuzasidan buyurishda e’tiborga olish lozim. Pregabalin qo‘llanganida doriga qaramlikni rivojlanishi to‘g‘risida xabarlar bor. Anamnezida doriga qaramlik bo‘lgan patsiyentlar pregabalinga qaramlik simptomlari yuz berishi yuzasidan sinchkov kuzatuvga muhtojdirlar. Entsefalopatiya holatlari, ayniqsa entsefalopatiyani rivojlanishiga olib kelishi mumkin bo‘lgan yo‘ldosh kasalliklari bo‘lgan patsiyentlarda aniqlangan. Pediatriyada ishlatilishi Pregabalin preparatining 12 yoshgacha bo‘lgan bolalarda va 17 yoshgacha bo‘lgan o‘smirlarda xavfsizligi va samaradorligi aniqlanmagan, shuning uchun preparatni ushbu toifa patsiyentlarda buyurish mumkin emas. Avtotransportni haydash va mexanizmlarni boshqarish qobiliyatiga ta’siri Pregabalin bosh aylanishi va uyquchanlikni chaqirishi mumkin va muvofiq ravishda avtomobilni boshqarish va murakkab texnikadan foydalanish qobiliyatiga ta’sir qilishi mumkin. Patsiyentlar preparatni qabul qilishga bo‘lgan shaxsiy reaktsiya aniqlanmagunicha avtomobilni boshqarmasliklari va murakkab texnikadan foydalanmasliklari yoki boshqa potentsial xavfli faoliyat turlarini bajarmasliklari lozim. Buyrak faoliyatini buzilishida qo‘llanishi Buyrak yetishmovchiligida preparatni ehtiyotkorlik bilan qo‘llash kerak. Buyrak faoliyatini buzilishi bo‘lgan patsiyentlarga dozani kreatinin klirensi (KK) ga bog‘liq holda tanlanadi. Jigar faoliyatini buzilishida qo‘llanishi Jigar faoliyatini buzilishi bo‘lgan bemorlarda dozani to‘g‘rilash talab qilinmaydi

Homiladorlik va laktasiya davrida

Homiladorlikda pregabalinni qo‘llanishi to‘g‘risida adekvat ma’lumotlar yo‘q. Hayvonlarda o‘tkazilgan eksperimental tadiqiqotlarda qo‘llanganida preparat reproduktiv faoliyatga toksik ta’sir ko‘rsatmagan. Shu sababli Regapen preparatini homiladorlarda faqat, agar ona uchun kutilgan foyda homila uchun mumkin bo‘lgan xavfdan aniq ustun bo‘lgan hollarda buyurish mumkin. Pregabalin bilan davolanishda reproduktiv yoshdagi ayollar kontratseptsiyaning adekvat usullaridan foydalanishlari kerak. Pregabalinni ayollarda ko‘krak suti bilan chiqarilishi to‘g‘risida ma’lumotlar yo‘q. Biroq eksperimental tadiqiqotlarda uni sut bilan chiqarilishi aniqlangan. Shu boisdan Regapen preparati bilan davolanish vaqtida emizish tavsiya qilinmaydi. Preparat bolalar ololmaydigan joyda saqlansin va yaroqlilik muddati o‘tganidan so‘ng ishlatilmasin.

Regapen qanday dori

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The information provided in of Regapen is based on data of another medicine with exactly the same composition as the Regapen. . Be careful and be sure to specify the information on the section in the instructions to the drug Regapen directly from the package or from the pharmacist at the pharmacy.

Pregabalin

Capsules; Substance; Substance-mixture; Substance-powder
Capsule, hard

Neuropathic pain

Regapen Milpharm is indicated for the treatment of peripheral and central neuropathic pain in adults.

Regapen Milpharm is indicated as adjunctive therapy in adults with partial seizures with or without secondary generalisation.

Generalised Anxiety Disorder

Regapen Milpharm is indicated for the treatment of Generalised Anxiety Disorder (GAD) in adults.

Regapen is indicated for the treatment of peripheral and central neuropathic pain in adults.

Regapen is indicated as adjunctive therapy in adults with partial seizures with or without secondary generalisation.

Generalised Anxiety Disorder

Regapen is indicated for the treatment of Generalised Anxiety Disorder (GAD) in adults.

Capsules; Substance; Substance-mixture; Substance-powder
Capsule, hard

The dose range is 150 to 600 mg per day given in either two or three divided doses.

Neuropathic pain

Regapen treatment can be started at a dose of 150 mg per day given as two or three divided doses. Based on individual patient response and tolerability, the dose may be increased to 300 mg per day after an interval of 3 to 7 days, and if needed, to a maximum dose of 600 mg per day after an additional 7-day interval.

Regapen treatment can be started with a dose of 150 mg per day given as two or three divided doses. Based on individual patient response and tolerability, the dose may be increased to 300 mg per day after 1 week. The maximum dose of 600 mg per day may be achieved after an additional week.

Generalised Anxiety Disorder

The dose range is 150 to 600 mg per day given as two or three divided doses. The need for treatment should be reassessed regularly.

Regapen treatment can be started with a dose of 150 mg per day. Based on individual patient response and tolerability, the dose may be increased to 300 mg per day after 1 week. Following an additional week the dose may be increased to 450 mg per day. The maximum dose of 600 mg per day may be achieved after an additional week.

Discontinuation of Regapen

In accordance with current clinical practice, if Regapen has to be discontinued, it is recommended this should be done gradually over a minimum of 1 week independent of the indication.

Renal impairment

Regapen is eliminated from the systemic circulation primarily by renal excretion as unchanged drug. As Regapen clearance is directly proportional to creatinine clearance , dose reduction in patients with compromised renal function must be individualised according to creatinine clearance (CLcr), as indicated in Table 1 determined using the following formula:

Regapen is removed effectively from plasma by haemodialysis (50% of drug in 4 hours). For patients receiving haemodialysis, the Regapen daily dose should be adjusted based on renal function. In addition to the daily dose, a supplementary dose should be given immediately following every 4 hour haemodialysis treatment (see Table 1).

Table 1. Regapen dose adjustment based on renal function

Total Regapen daily dose *

Once Daily or BID

Supplementary dosage following haemodialysis (mg)

TID = Three divided doses

BID = Two divided doses

* Total daily dose (mg/day) should be divided as indicated by dose regimen to provide mg/dose

+ Supplementary dose is a single additional dose

Hepatic impairment

No dose adjustment is required for patients with hepatic impairment.

Paediatric population

25 – 50 (1.25-2.5 ml)

Once Daily or BID

Supplementary dose following haemodialysis (mg)

TID = Three divided doses

BID = Two divided doses

* Total daily dose (mg/day) should be divided as indicated by dose regimen to provide mg/dose

+ Supplementary dose is a single additional dose

No dose adjustment is required for patients with hepatic impairment.

Capsules; Substance; Substance-mixture; Substance-powder
Capsule, hard

Diabetic patients

In accordance with current clinical practice, some diabetic patients who gain weight on Regapen treatment may need to adjust hypoglycaemic medicinal products.

Hypersensitivity reactions

There have been reports in the postmarketing experience of hypersensitivity reactions, including cases of angioedema. Regapen should be discontinued immediately if symptoms of angioedema, such as facial, perioral, or upper airway swelling occur.

Dizziness, somnolence, loss of consciousness, confusion and mental impairment

Regapen treatment has been associated with dizziness and somnolence, which could increase the occurrence of accidental injury (fall) in the elderly population. There have also been post-marketing reports of loss of consciousness, confusion and mental impairment. Therefore, patients should be advised to exercise caution until they are familiar with the potential effects of the medicinal product.

Vision-related effects

In controlled trials, a higher proportion of patients treated with Regapen reported blurred vision than did patients treated with placebo which resolved in a majority of cases with continued dosing. In the clinical studies where ophthalmologic testing was conducted, the incidence of visual acuity reduction and visual field changes was greater in Regapen-treated patients than in placebo-treated patients; the incidence of fundoscopic changes was greater in placebo-treated patients.

In the post-marketing experience, visual adverse reactions have also been reported, including loss of vision, visual blurring or other changes of visual acuity, many of which were transient.

Discontinuation of Regapen may result in resolution or improvement of these visual symptoms.

Renal failure

Cases of renal failure have been reported and in some cases discontinuation of Regapen did show reversibility of this adverse reaction.

Withdrawal of concomitant antiepileptic medicinal products

There are insufficient data for the withdrawal of concomitant antiepileptic medicinal products, once seizure control with Regapen in the add-on situation has been reached, in order to reach monotherapy on Regapen.

Withdrawal symptoms

After discontinuation of short-term and long-term treatment with Regapen withdrawal symptoms have been observed in some patients. The following events have been mentioned: insomnia, headache, nausea, anxiety, diarrhoea, flu syndrome, nervousness, depression, pain, convulsion, hyperhidrosis and dizziness, suggestive of physical dependence. The patient should be informed about this at the start of the treatment.

Convulsions, including status epilepticus and grand mal convulsions, may occur during Regapen use or shortly after discontinuing Regapen.

Concerning discontinuation of long-term treatment of Regapen, data suggest that the incidence and severity of withdrawal symptoms may be dose-related.

Congestive heart failure

There have been post-marketing reports of congestive heart failure in some patients receiving Regapen. These reactions are mostly seen in elderly cardiovascular compromised patients during Regapen treatment for a neuropathic indication. Regapen should be used with caution in these patients. Discontinuation of Regapen may resolve the reaction.

Treatment of central neuropathic pain due to spinal cord injury

In the treatment of central neuropathic pain due to spinal cord injury the incidence of adverse reactions in general, central nervous system adverse reactions and especially somnolence was increased. This may be attributed to an additive effect due to concomitant medicinal products (e.g. anti-spasticity agents) needed for this condition. This should be considered when prescribing Regapen in this condition.

Suicidal ideation and behaviour

Suicidal ideation and behaviour have been reported in patients treated with anti-epileptic agents in several indications. A meta-analysis of randomised placebo controlled studies of anti-epileptic drugs has also shown a small increased risk of suicidal ideation and behaviour. The mechanism of this risk is not known and the available data do not exclude the possibility of an increased risk for Regapen.

Therefore patients should be monitored for signs of suicidal ideation and behaviours and appropriate treatment should be considered. Patients (and caregivers of patients) should be advised to seek medical advice should signs of suicidal ideation or behaviour emerge.

Reduced lower gastrointestinal tract function

There are post-marketing reports of events related to reduced lower gastrointestinal tract function (e.g., intestinal obstruction, paralytic ileus, constipation) when Regapen was co-administered with medications that have the potential to produce constipation, such as opioid analgesics. When Regapen and opioids will be used in combination, measures to prevent constipation may be considered (especially in female patients and elderly).

Misuse, abuse potential or dependence

Cases of misuse, abuse and dependence have been reported. Caution should be exercised in patients with a history of substance abuse and the patient should be monitored for symptoms of Regapen misuse, abuse or dependence (development of tolerance, dose escalation, drug-seeking behaviour have been reported).

Encephalopathy

Cases of encephalopathy have been reported, mostly in patients with underlying conditions that may precipitate encephalopathy.

In accordance with current clinical practice, some diabetic patients who gain weight on pregabalin treatment may need to adjust hypoglycaemic medicinal products.

There have been reports in the postmarketing experience of hypersensitivity reactions, including cases of angioedema. Pregabalin should be discontinued immediately if symptoms of angioedema, such as facial, perioral, or upper airway swelling occur.

Dizziness, somnolence, loss of consciousness, confusion and mental impairment

Pregabalin treatment has been associated with dizziness and somnolence, which could increase the occurrence of accidental injury (fall) in the elderly population. There have also been postmarketing reports of loss of consciousness, confusion and mental impairment. Therefore, patients should be advised to exercise caution until they are familiar with the potential effects of the medicinal product.

In controlled trials, a higher proportion of patients treated with pregabalin reported blurred vision than did patients treated with placebo which resolved in a majority of cases with continued dosing. In the clinical studies where ophthalmologic testing was conducted, the incidence of visual acuity reduction and visual field changes was greater in pregabalin-treated patients than in placebo-treated patients; the incidence of fundoscopic changes was greater in placebo-treated patients.

In the postmarketing experience, visual adverse reactions have also been reported, including loss of vision, visual blurring or other changes of visual acuity, many of which were transient. Discontinuation of pregabalin may result in resolution or improvement of these visual symptoms.

Cases of renal failure have been reported and in some cases discontinuation of pregabalin did show reversibility of this adverse reaction.

Withdrawal of concomitant anti-epileptic medicinal products

There are insufficient data for the withdrawal of concomitant anti-epileptic medicinal products, once seizure control with pregabalin in the add-on situation has been reached, in order to reach monotherapy on pregabalin.

After discontinuation of short-term and long-term treatment with pregabalin, withdrawal symptoms have been observed in some patients. The following events have been mentioned: insomnia, headache, nausea, anxiety, diarrhoea, flu syndrome, nervousness, depression, pain, convulsion, hyperhidrosis and dizziness, suggestive of physical dependence. The patient should be informed about this at the start of the treatment.

Convulsions, including status epilepticus and grand mal convulsions, may occur during pregabalin use or shortly after discontinuing pregabalin.

Concerning discontinuation of long-term treatment of pregabalin, data suggest that the incidence and severity of withdrawal symptoms may be dose-related.

Congestive heart failure

There have been postmarketing reports of congestive heart failure in some patients receiving pregabalin. These reactions are mostly seen in elderly cardiovascular compromised patients during pregabalin treatment for a neuropathic indication. Pregabalin should be used with caution in these patients. Discontinuation of pregabalin may resolve the reaction.

Treatment of central neuropathic pain due to spinal cord injury

Suicidal ideation and behaviour

Reduced lower gastrointestinal tract function

There are postmarketing reports of events related to reduced lower gastrointestinal tract function (e.g. intestinal obstruction, paralytic ileus, constipation) when pregabalin was co-administered with medications that have the potential to produce constipation, such as opioid analgesics. When pregabalin and opioids will be used in combination, measures to prevent constipation may be considered (especially in female patients and elderly).

Misuse, abuse potential or dependence

Cases of misuse, abuse and dependence have been reported. Caution should be exercised in patients with a history of substance abuse and the patient should be monitored for symptoms of pregabalin misuse, abuse or dependence (development of tolerance, dose escalation, drug-seeking behaviour have been reported).

Cases of encephalopathy have been reported, mostly in patients with underlying conditions that may precipitate encephalopathy.

Excipients which may cause allergic reactions

Regapen oral solution contains methyl parahydroxybenzoate and propyl parahydroxybenzoate which may cause allergic reactions (possibly delayed).

Effects on ability to drive and use machines

The information provided in Effects on ability to drive and use machines of Regapen is based on data of another medicine with exactly the same composition as the Regapen. . Be careful and be sure to specify the information on the section Effects on ability to drive and use machines in the instructions to the drug Regapen directly from the package or from the pharmacist at the pharmacy.

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Regapen Milpharm may have minor or moderate influence on the ability to drive and use machines. Regapen Milpharm may cause dizziness and somnolence and therefore may influence the ability to drive or use machines. Patients are advised not to drive, operate complex machinery or engage in other potentially hazardous activities until it is known whether this medicinal product affects their ability to perform these activities.

Regapen may have minor or moderate influence on the ability to drive and use machines. Regapen may cause dizziness and somnolence and therefore may influence the ability to drive or use machines. Patients are advised not to drive, operate complex machinery or engage in other potentially hazardous activities until it is known whether this medicinal product affects their ability to perform these activities.

Undesirable effects

The information provided in Undesirable effects of Regapen is based on data of another medicine with exactly the same composition as the Regapen. . Be careful and be sure to specify the information on the section Undesirable effects in the instructions to the drug Regapen directly from the package or from the pharmacist at the pharmacy.

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The Regapen clinical programme involved over 8900 patients exposed to Regapen, of whom over 5600 were in double-blind placebo controlled trials. The most commonly reported adverse reactions were dizziness and somnolence. Adverse reactions were usually mild to moderate in intensity. In all controlled studies, the discontinuation rate due to adverse reactions was 12% for patients receiving Regapen and 5% for patients receiving placebo. The most common adverse reactions resulting in discontinuation from Regapen treatment groups were dizziness and somnolence.

In the table 2 below all adverse reactions, which occurred at an incidence greater than placebo and in more than one patient, are listed by class and frequency (very common (>1/10); common (>1/100 to 1/1,000 to 1/10,000 to

The adverse reactions listed may also be associated with the underlying disease and/or concomitant medicinal products.

In the treatment of central neuropathic pain due to spinal cord injury the incidence of adverse reactions in general, CNS adverse reactions and especially somnolence was increased.

Additional reactions reported from post-marketing experience are included in italics in the list below.

Table 2. Regapen adverse drug reactions

System Organ Class

Adverse drug reactions

Infections and infestations

Blood and lymphatic system disorders

Immune system disorders

Angioedema, allergic reaction

Metabolism and nutrition disorders

Psychiatric disorders

Euphoric mood, confusion, irritability, libido decreased, disorientation, insomnia

Hallucination, panic attack, restlessness, agitation, depression, depressed mood, elevated mood , aggression, mood swings, depersonalisation, word finding difficulty, abnormal dreams, libido increased, anorgasmia, apathy

Nervous system disorders

Dizziness, somnolence, headache

Ataxia, coordination abnormal, tremor, dysarthria, amnesia, memory impairment, disturbance in attention, paraesthesia, hypoaesthesia, sedation, balance disorder, lethargy

Syncope, stupor, myoclonus, loss of consciousness, psychomotor hyperactivity, dyskinesia, dizziness postural, intention tremor, nystagmus, cognitive disorder, mental impairment, speech disorder, hyporeflexia, hyperaesthesia, burning sensation, ageusia, malaise

Convulsions , hypokinesia, parosmia, dysgraphia

Eye disorders

Vision blurred, diplopia

Peripheral vision loss, Visual disturbance, eye swelling, visual field defect, visual acuity reduced, eye pain, asthenopia, photopsia, dry eye, lacrimation increased, eye irritation,

Vision loss, keratitis,oscillopsia, altered visual depth perception, mydriasis, strabismus, visual brightness

Ear and labyrinth disorders

Cardiac disorders

Tachycardia, atrioventricular block first degree, sinus bradycardia, Congestive heart failure

QT prolongation , sinus tachycardia, sinus arrhythmia

Vascular disorders

Flushing, hot flushes, hypotension, hypertension, peripheral coldness

Respiratory, thoracic and mediastinal disorders

Dyspnoea, epistaxis, cough, nasal congestion, rhinitis, snoring, nasal dryness

Pulmonary oedema, throat tightness

Gastrointestinal disorders

Vomiting, nausea, dry mouth, constipation, diarrhoea,flatulence, abdominal distension

Gastrooesophageal reflux disease, salivary hypersecretion, hypoaesthesia oral

Ascites, pancreatitis, dysphagia, Swollen tongue

Skin and subcutaneous tissue disorders

Rash papular, hyperhidrosis, urticaria, pruritus

Stevens Johnson syndrome, cold sweat

Musculoskeletal and connective tissue disorders

Muscle cramp, arthralgia, back pain, pain in limb, cervical spasm

Joint swelling, myalgia , muscle twitching, neck pain, muscle stiffness

Renal and urinary disorders

Urinary incontinence, dysuria

Renal failure, oliguria, urinary retention

Reproductive system and breast disorders

Ejaculation delayed, sexual dysfunction, dysmenorrhoea, breast pain

Amenorrhoea, breast discharge, breast enlargement, gynaecomastia

General disorders and administration site conditions

Gait abnormal, feeling drunk, fatigue, oedema peripheral, oedema, fall, feeling abnormal

Generalised oedema,pyrexia, face oedema, chest tightness, pain, thirst, chills, asthenia

Investigations

Blood creatine phosphokinase increased, alanine aminotransferase increased, aspartate aminotransferase increased, blood glucose increased, platelet count decreased, blood creatinine increased , blood potassium decreased, weight decreased.

White blood cell count decreased

After discontinuation of short-term and long-term treatment with Regapen withdrawal symptoms have been observed in some patients. The following reactions have been mentioned: insomnia, headache, nausea, anxiety, diarrhoea, flu syndrome, convulsions, nervousness, depression, pain, hyperhidrosis and dizziness suggestive of physical dependence. The patient should be informed about this at the start of the treatment.

Concerning discontinuation of long-term treatment of Regapen, data suggest that the incidence and severity of withdrawal symptoms may be dose-related.

The Regapen safety profile observed in two paediatric studies (pharmacokinetic and tolerability study, n=65; 1 year open label follow on safety study, n=54) was similar to that observed in the adult studies.

Reporting of suspected adverse reactions

Reporting suspected adverse reactions after authorisation of the medicinal product is important. It allows continued monitoring of the benefit/risk balance of the medicinal product. Healthcare professionals are asked to report any suspected adverse reactions via the Yellow Card Scheme at: www.mhra.gov.uk/yellowcard.

The pregabalin clinical programme involved over 8,900 patients exposed to pregabalin, of whom over 5,600 were in double-blind placebo controlled trials. The most commonly reported adverse reactions were dizziness and somnolence. Adverse reactions were usually mild to moderate in intensity. In all controlled studies, the discontinuation rate due to adverse reactions was 12% for patients receiving pregabalin and 5% for patients receiving placebo. The most common adverse reactions resulting in discontinuation from pregabalin treatment groups were dizziness and somnolence.

In table 2 below all adverse reactions, which occurred at an incidence greater than placebo and in more than one patient, are listed by class and frequency (very common (> 1/10); common (> 1/100 to < 1/10); uncommon (>1/1,000 to < 1/100); rare (>1/10,000 to < 1/1,000); very rare (< 1/10,000), not known (cannot be estimated from the available data).

Within each frequency grouping, undesirable effects are presented in order of decreasing seriousness.

The adverse reactions listed may also be associated with the underlying disease and/or concomitant medicinal products.

In the treatment of central neuropathic pain due to spinal cord injury the incidence of adverse reactions in general, CNS adverse reactions and especially somnolence was increased.

Additional reactions reported from postmarketing experience are included in italics in the list below.

Table 2. Pregabalin Adverse Drug Reactions

System Organ Class

Adverse drug reactions

Infections and infestations

Blood and lymphatic system disorders

Immune system disorders

Hypersensitivity

Angioedema, allergic reaction

Metabolism and nutrition disorders

Psychiatric disorders

Euphoric mood, confusion, irritability, disorientation, insomnia, libido decreased

Hallucination, panic attack, restlessness, agitation, depression, depressed mood, elevated mood, aggression, mood swings, depersonalisation, word finding difficulty, abnormal dreams, libido increased, anorgasmia, apathy

Nervous system disorders

Dizziness, somnolence, headache

Ataxia, coordination abnormal, tremor, dysarthria, amnesia, memory impairment, disturbance in attention, paraesthesia, hypoaesthesia, sedation, balance disorder, lethargy

Syncope, stupor, myoclonus, loss of consciousness, psychomotor hyperactivity, dyskinesia, dizziness postural, intention tremor, nystagmus, cognitive disorder, mental impairment, speech disorder, hyporeflexia, hyperaesthesia, burning sensation, ageusia, malaise

Convulsions, parosmia, hypokinesia, dysgraphia

Eye disorders

Vision blurred, diplopia

Peripheral vision loss, visual disturbance, eye swelling, visual field defect, visual acuity reduced, eye pain, asthenopia, photopsia, dry eye, lacrimation increased, eye irritation

Vision loss, keratitis, oscillopsia, altered visual depth perception, mydriasis, strabismus, visual brightness

Ear and labyrinth disorders

Cardiac disorders

Tachycardia, atrioventricular block first degree, sinus bradycardia, congestive heart failure

QT prolongation, sinus tachycardia, sinus arrhythmia

Vascular disorders

Hypotension, hypertension, hot flushes, flushing, peripheral coldness

Respiratory, thoracic and mediastinal disorders

Dyspnoea, epistaxis, cough, nasal congestion, rhinitis, snoring, nasal dryness

Pulmonary oedema, throat tightness

Gastrointestinal disorders

Vomiting, nausea, constipation, diarrhoea, flatulence, abdominal distension, dry mouth

Gastrooesophageal reflux disease, salivary hypersecretion, hypoaesthesia oral

Ascites, pancreatitis, swollen tongue, dysphagia

Hepatobiliary disorders

Elevated liver enzymes*

Hepatic failure, hepatitis

Skin and subcutaneous tissue disorders

Rash papular, urticaria, hyperhidrosis, pruritus

Stevens Johnson syndrome, cold sweat

Musculoskeletal and connective tissue disorders

Muscle cramp, arthralgia, back pain, pain in limb, cervical spasm

Joint swelling, myalgia, muscle twitching, neck pain, muscle stiffness

Renal and urinary disorders

Urinary incontinence, dysuria

Renal failure, oliguria, urinary retention

Reproductive system and breast disorders

Sexual dysfunction, ejaculation delayed, dysmenorrhoea, breast pain

Amenorrhoea, breast discharge, breast enlargement, gynaecomastia

General disorders and administration site conditions

Oedema peripheral, oedema, gait abnormal, fall, feeling drunk, feeling abnormal, fatigue

Generalised oedema, face oedema, chest tightness, pain, pyrexia, thirst, chills, asthenia

Investigations

Blood creatine phosphokinase increased, blood glucose increased, platelet count decreased, blood creatinine increased, blood potassium decreased, weight decreased

White blood cell count decreased

* Alanine aminotransferase increased (ALT) and aspartate aminotransferase increased (AST).

After discontinuation of short-term and long-term treatment with pregabalin withdrawal symptoms have been observed in some patients. The following reactions have been mentioned: insomnia, headache, nausea, anxiety, diarrhoea, flu syndrome, convulsions, nervousness, depression, pain, hyperhidrosis and dizziness, suggestive of physical dependence. The patient should be informed about this at the start of the treatment.

Concerning discontinuation of long-term treatment of pregabalin, data suggest that the incidence and severity of withdrawal symptoms may be dose-related.

The pregabalin safety profile observed in three paediatric studies in patients with partial seizures with or without secondary generalization (12-week efficacy and safety study in patients with partial onset seizures, n=295; pharmacokinetic and tolerability study, n=65; and 1 year open label follow on safety study, n=54) was similar to that observed in the adult studies of patients with epilepsy. The most common adverse events observed in the 12-week study with pregabalin treatment were somnolence, pyrexia, upper respiratory tract infection, increased appetite, weight increased, and nasopharyngitis.

Reporting of suspected adverse reactions

Yellow Card Scheme at: www.mhra.gov.uk/yellowcard

HPRA Pharmacovigilance, Earlsfort Terrace, IRL – Dublin 2; Tel: +353 1 6764971; Fax: +353 1 6762517. Website: www.hpra.ie; E-mail: [email protected]

The information provided in Overdose of Regapen is based on data of another medicine with exactly the same composition as the Regapen. . Be careful and be sure to specify the information on the section Overdose in the instructions to the drug Regapen directly from the package or from the pharmacist at the pharmacy.

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In the post-marketing experience, the most commonly reported adverse reactions observed when Regapen was taken in overdose included somnolence, confusional state, agitation, and restlessness. Seizures were also reported.

In rare occasions, cases of coma have been reported.

Treatment of Regapen overdose should include general supportive measures and may include haemodialysis if necessary.

In the postmarketing experience, the most commonly reported adverse reactions observed when pregabalin was taken in overdose included somnolence, confusional state, agitation, and restlessness. Seizures were also reported.

In rare occasions, cases of coma have been reported.

Treatment of pregabalin overdose should include general supportive measures and may include haemodialysis if necessary.

Pharmacodynamic properties

The information provided in Pharmacodynamic properties of Regapen is based on data of another medicine with exactly the same composition as the Regapen. . Be careful and be sure to specify the information on the section Pharmacodynamic properties in the instructions to the drug Regapen directly from the package or from the pharmacist at the pharmacy.

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Pharmacotherapeutic group: Antiepileptics, other antiepileptics ATC code: N03AX16

The active substance, Regapen, is a gamma-aminobutyric acid analogue ((S)-3-(aminomethyl)-5- methylhexanoic acid).

Mechanism of action

Regapen binds to an auxiliary subunit (Î±2-Î´ protein) of voltage-gated calcium channels in the central nervous system.

Clinical Efficacy and safety

Neuropathic pain

Efficacy has been shown in trials in diabetic neuropathy, post herpetic neuralgia and spinal cord injury. Efficacy has not been studied in other models of neuropathic pain.

Regapen has been studied in 10 controlled clinical trials of up to 13 weeks with twice a day dosing (BID) and up to 8 weeks with three times a day (TID) dosing. Overall, the safety and efficacy profiles for BID and TID dosing regimens were similar.

In clinical trials up to 12 weeks for both peripheral and central neuropathic pain, a reduction in pain was seen by week 1 and was maintained throughout the treatment period.

In controlled clinical trials in peripheral neuropathic pain 35% of the Regapen treated patients and 18% of the patients on placebo had a 50% improvement in pain score. For patient’s not experiencing somnolence, such an improvement was observed in 33% of patients treated with Regapen and 18% of patients on placebo. For patients who experienced somnolence the responder rates were 48% on Regapen and 16% on placebo.

In the controlled clinical trial in central neuropathic pain 22% of the Regapen treated patients and 7% of the patients on placebo had a 50% improvement in pain score.

Regapen has been studied in 3 controlled clinical trials of 12 week duration with either twice a day dosing (BID) or three times a day (TID) dosing. Overall, the safety and efficacy profiles for BID and TID dosing regimens were similar.

A reduction in seizure frequency was observed by Week 1.

The efficacy and safety of Regapen as adjunctive treatment for epilepsy in paediatric patients below the age of 12 and adolescents has not been established. The adverse events observed in a pharmacokinetic and tolerability study that enrolled patients from 3 months to 16 years of age (n=65) were similar to those observed in adults. Results of a 1 year open label safety study in 54 paediatric patients from 3 months to 16 years of age with epilepsy indicate that the adverse events of pyrexia and upper respiratory infections were observed more frequently than in adult studies.

Monotherapy (newly diagnosed patients)

Regapen has been studied in 1 controlled clinical trial of 56 week duration with twice a day dosing (BID). Regapen did not achieve non-inferiority to lamotrigine based on the 6-month seizure freedom endpoint. Regapen and lamotrigine were similarly safe and well tolerated.

Generalised Anxiety Disorder

Regapen has been studied in 6 controlled trials of 4-6 week duration, an elderly study of 8 week duration and a long-term relapse prevention study with a double blind relapse prevention phase of 6 months duration.

Relief of the symptoms of GAD as reflected by the Hamilton Anxiety Rating Scale (HAM-A) was observed by Week 1.

In controlled clinical trials (4-8 week duration) 52% of the Regapen treated patients and 38% of the patients on placebo had at least a 50% improvement in HAM-A total score from baseline to endpoint.

In controlled trials, a higher proportion of patients treated with Regapen reported blurred vision than did patients treated with placebo which resolved in a majority of cases with continued dosing. Ophthamologic testing (including visual acuity testing, formal visual field testing and dilated funduscopic examination) was conducted in over 3600 patients within controlled clinical trials. In these patients, visual acuity was reduced in 6.5% of patients treated with Regapen, and 4.8% of placebo-treated patients. Visual field changes were detected in 12.4% of Regapen-treated, and 11.7% of placebo-treated patients. Funduscopic changes were observed in 1.7% of Regapen-treated and 2.1% of placebo-treated patients.

Pharmacotherapeutic group: Anti-epileptics, other anti-epileptics ATC code: N03AX16

The active substance, pregabalin, is a gamma-aminobutyric acid analogue [(S)-3-(aminomethyl)-5-methylhexanoic acid].

Mechanism of action

Pregabalin binds to an auxiliary subunit (Î±₂-Î´ protein) of voltage-gated calcium channels in the central nervous system.

Clinical efficacy and safety

Neuropathic pain

Efficacy has been shown in trials in diabetic neuropathy, post herpetic neuralgia and spinal cord injury. Efficacy has not been studied in other models of neuropathic pain.

Pregabalin has been studied in 10 controlled clinical trials of up to 13 weeks with twice a day dosing (BID) and up to 8 weeks with three times a day (TID) dosing. Overall, the safety and efficacy profiles for BID and TID dosing regimens were similar.

In clinical trials up to 12 weeks for both peripheral and central neuropathic pain, a reduction in pain was seen by Week 1 and was maintained throughout the treatment period.

In controlled clinical trials in peripheral neuropathic pain 35% of the pregabalin treated patients and 18% of the patients on placebo had a 50% improvement in pain score. For patients not experiencing somnolence, such an improvement was observed in 33% of patients treated with pregabalin and 18% of patients on placebo. For patients who experienced somnolence the responder rates were 48% on pregabalin and 16% on placebo.

In the controlled clinical trial in central neuropathic pain 22% of the pregabalin treated patients and 7% of the patients on placebo had a 50% improvement in pain score.

Pregabalin has been studied in 3 controlled clinical trials of 12 week duration with BID or TID dosing. Overall, the safety and efficacy profiles for BID and TID dosing regimens were similar.

A reduction in seizure frequency was observed by Week 1.

The efficacy and safety of pregabalin as adjunctive treatment for epilepsy in paediatric patients below the age of 12 and adolescents has not been established. The adverse events observed in a pharmacokinetic and tolerability study that enrolled patients from 3 months to 16 years of age (n=65) with partial onset seizures were similar to those observed in adults. Results of a 12-week placebo-controlled study of 295 paediatric patients aged 4 to 16 years performed to evaluate the efficacy and safety of pregabalin as adjunctive therapy for the treatment of partial onset seizures and a 1 year open label safety study in 54 paediatric patients from 3 months to 16 years of age with epilepsy indicate that the adverse events of pyrexia and upper respiratory infections were observed more frequently than in adult studies of patients with epilepsy.

In the 12-week placebo-controlled study, paediatric patients were assigned to pregabalin 2.5 mg/kg/day (maximum, 150 mg/day), pregabalin 10/mg/kg/day (maximum, 600 mg/day), or placebo. The percentage of subjects with at least a 50% reduction in partial onset seizures as compared to baseline was 40.6% of subjects treated with pregabalin 10 mg/kg/day group (p=0.0068 versus placebo), 29.1% of subjects treated with pregabalin 2.5 mg/kg/day (p=0.2600 versus placebo) and 22.6% of those receiving placebo.

Monotherapy (newly diagnosed patients)

Pregabalin has been studied in 1 controlled clinical trial of 56 week duration with BID dosing. Pregabalin did not achieve non-inferiority to lamotrigine based on the 6-month seizure freedom endpoint. Pregabalin and lamotrigine were similarly safe and well tolerated.

Generalised Anxiety Disorder

Pregabalin has been studied in 6 controlled trials of 4-6 week duration, an elderly study of 8 week duration and a long-term relapse prevention study with a double-blind relapse prevention phase of 6 months duration.

Relief of the symptoms of GAD as reflected by the Hamilton Anxiety Rating Scale (HAM-A) was observed by Week 1.

In controlled clinical trials (4-8 week duration) 52% of the pregabalin treated patients and 38% of the patients on placebo had at least a 50% improvement in HAM-A total score from baseline to endpoint.

In controlled trials, a higher proportion of patients treated with pregabalin reported blurred vision than did patients treated with placebo which resolved in a majority of cases with continued dosing. Ophthamologic testing (including visual acuity testing, formal visual field testing and dilated funduscopic examination) was conducted in over 3600 patients within controlled clinical trials. In these patients, visual acuity was reduced in 6.5% of patients treated with pregabalin, and 4.8% of placebo-treated patients. Visual field changes were detected in 12.4% of pregabalin-treated, and 11.7% of placebo-treated patients. Funduscopic changes were observed in 1.7% of pregabalin-treated and 2.1% of placebo-treated patients.

Pharmacokinetic properties

The information provided in Pharmacokinetic properties of Regapen is based on data of another medicine with exactly the same composition as the Regapen. . Be careful and be sure to specify the information on the section Pharmacokinetic properties in the instructions to the drug Regapen directly from the package or from the pharmacist at the pharmacy.

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Regapen steady-state pharmacokinetics are similar in healthy volunteers, patients with epilepsy receiving anti-epileptic drugs and patients with chronic pain.

Regapen is rapidly absorbed when administered in the fasted state, with peak plasma concentrations occurring within 1 hour following both single and multiple dose administration. Regapen oral bioavailability is estimated to be > 90% and is independent of dose. Following repeated administration, steady state is achieved within 24 to 48 hours. The rate of Regapen absorption is decreased when given with food resulting in a decrease in Cmax by approximately 25-30% and a delay in tmax to approximately 2.5 hours. However, administration of Regapen with food has no clinically significant effect on the extent of Regapen absorption.

In preclinical studies, Regapen has been shown to cross the blood brain barrier in mice, rats, and monkeys. Regapen has been shown to cross the placenta in rats and is present in the milk of lactating rats. In humans, the apparent volume of distribution of Regapen following oral administration is approximately 0.56 l/kg. Regapen is not bound to plasma proteins.

Regapen undergoes negligible metabolism in humans. Following a dose of radiolabelled Regapen, approximately 98% of the radioactivity recovered in the urine was unchanged Regapen. The N- methylated derivative of Regapen, the major metabolite of Regapen found in urine, accounted for 0.9% of the dose. In preclinical studies, there was no indication of racemisation of Regapen S- enantiomer to the R-enantiomer.

Regapen is eliminated from the systemic circulation primarily by renal excretion as unchanged drug. Regapen mean elimination half-life is 6.3 hours. Regapen plasma clearance and renal clearance are directly proportional to creatinine clearance.

Dose adjustment in patients with reduced renal function or undergoing haemodialysis is necessary.

Clinical trials indicate that gender does not have a clinically significant influence on the plasma concentrations of Regapen.

Regapen clearance is directly proportional to creatinine clearance. In addition, Regapen is effectively removed from plasma by haemodialysis (following a 4 hour haemodialysis treatment plasma Regapen concentrations are reduced by approximately 50%). Because renal elimination is the major elimination pathway, dose reduction in patients with renal impairment and dose supplementation following haemodialysis is necessary.

No specific pharmacokinetic studies were carried out in patients with impaired liver function. Since Regapen does not undergo significant metabolism and is excreted predominantly as unchanged drug in the urine, impaired liver function would not be expected to significantly alter Regapen plasma concentrations.

Regapen pharmacokinetics were evaluated in paediatric patients with epilepsy (age groups: 1 to 23 months, 2 to 6 years, 7 to 11 years and 12 to 16 years) at dose levels of 2.5, 5, 10 and 15 mg/kg/day in a pharmacokinetic and tolerability study.

After oral administration of Regapen in paediatric patients in the fasted state, in general, time to reach peak plasma concentration was similar across the entire age group and occurred 0.5 hours to 2 hours postdose.

Regapen Cmax and AUC parameters increased in a linear manner with increasing dose within each age group. The AUC was lower by 30% in paediatric patients below a weight of 30 kg due to an increased body weight adjusted clearance of 43% for these patients in comparison to patients weighing >30 kg.

Regapen terminal half-life averaged about 3 to 4 hours in paediatric patients up to 6 years of age, and 4 to 6 hours in those 7 years of age and older.

Population pharmacokinetic analysis showed that creatinine clearance was a significant covariate of Regapen oral clearance, body weight was a significant covariate of Regapen apparent oral volume of distribution, and these relationships were similar in paediatric and adult patients.

Regapen pharmacokinetics in patients younger than 3 months old have not been studied.

Regapen clearance tends to decrease with increasing age. This decrease in Regapen oral clearance is consistent with decreases in creatinine clearance associated with increasing age. Reduction of Regapen dose may be required in patients who have age related compromised renal function.

The pharmacokinetics of 150 mg Regapen given every 12 hours (300 mg daily dose) was evaluated in 10 lactating women who were at least 12 weeks postpartum. Lactation had little to no influence on Regapen pharmacokinetics. Regapen was excreted into breast milk with average steady-state concentrations approximately 76% of those in maternal plasma. The estimated infant dose from breast milk (assuming mean milk consumption of 150 ml/kg/day) of women receiving 300 mg/day or the maximum dose of 600 mg/day would be 0.31 or 0.62 mg/kg/day, respectively. These estimated doses are approximately 7% of the total daily maternal dose on a mg/kg basis.

Pregabalin steady-state pharmacokinetics are similar in healthy volunteers, patients with epilepsy receiving anti-epileptic drugs and patients with chronic pain.

Pregabalin is rapidly absorbed when administered in the fasted state, with peak plasma concentrations occurring within 1 hour following both single and multiple dose administration. Pregabalin oral bioavailability is estimated to be > 90% and is independent of dose. Following repeated administration, steady state is achieved within 24 to 48 hours. The rate of pregabalin absorption is decreased when given with food resulting in a decrease in C_max by approximately 25-30% and a delay in t_max to approximately 2.5 hours. However, administration of pregabalin with food has no clinically significant effect on the extent of pregabalin absorption.

In preclinical studies, pregabalin has been shown to cross the blood brain barrier in mice, rats, and monkeys. Pregabalin has been shown to cross the placenta in rats and is present in the milk of lactating rats. In humans, the apparent volume of distribution of pregabalin following oral administration is approximately 0.56 l/kg. Pregabalin is not bound to plasma proteins.

Pregabalin undergoes negligible metabolism in humans. Following a dose of radiolabelled pregabalin, approximately 98% of the radioactivity recovered in the urine was unchanged pregabalin. The N-methylated derivative of pregabalin, the major metabolite of pregabalin found in urine, accounted for 0.9% of the dose. In preclinical studies, there was no indication of racemisation of pregabalin S-enantiomer to the R-enantiomer.

Pregabalin is eliminated from the systemic circulation primarily by renal excretion as unchanged drug.

Pregabalin mean elimination half-life is 6.3 hours. Pregabalin plasma clearance and renal clearance are directly proportional to creatinine clearance.

Dose adjustment in patients with reduced renal function or undergoing haemodialysis is necessary.

Clinical trials indicate that gender does not have a clinically significant influence on the plasma concentrations of pregabalin.

Pregabalin clearance is directly proportional to creatinine clearance. In addition, pregabalin is effectively removed from plasma by haemodialysis (following a 4 hour haemodialysis treatment plasma pregabalin concentrations are reduced by approximately 50%). Because renal elimination is the major elimination pathway, dose reduction in patients with renal impairment and dose supplementation following haemodialysis is necessary.

No specific pharmacokinetic studies were carried out in patients with impaired liver function. Since pregabalin does not undergo significant metabolism and is excreted predominantly as unchanged drug in the urine, impaired liver function would not be expected to significantly alter pregabalin plasma concentrations.

Pregabalin pharmacokinetics were evaluated in paediatric patients with epilepsy (age groups: 1 to 23 months, 2 to 6 years, 7 to 11 years and 12 to 16 years) at dose levels of 2.5, 5, 10 and 15 mg/kg/day in a pharmacokinetic and tolerability study.

After oral administration of pregabalin in paediatric patients in the fasted state, in general, time to reach peak plasma concentration was similar across the entire age group and occurred 0.5 hours to 2 hours postdose.

Pregabalin C_max and AUC parameters increased in a linear manner with increasing dose within each age group. The AUC was lower by 30% in paediatric patients below a weight of 30 kg due to an increased body weight adjusted clearance of 43% for these patients in comparison to patients weighing >30 kg.

Pregabalin terminal half-life averaged about 3 to 4 hours in paediatric patients up to 6 years of age, and 4 to 6 hours in those 7 years of age and older.

Population pharmacokinetic analysis showed that creatinine clearance was a significant covariate of pregabalin oral clearance, body weight was a significant covariate of pregabalin apparent oral volume of distribution, and these relationships were similar in paediatric and adult patients.

Pregabalin pharmacokinetics in patients younger than 3 months old have not been studied.

Pregabalin clearance tends to decrease with increasing age. This decrease in pregabalin oral clearance is consistent with decreases in creatinine clearance associated with increasing age. Reduction of pregabalin dose may be required in patients who have age related compromised renal function.

The pharmacokinetics of 150 mg pregabalin given every 12 hours (300 mg daily dose) was evaluated in 10 lactating women who were at least 12 weeks postpartum. Lactation had little to no influence on pregabalin pharmacokinetics. Pregabalin was excreted into breast milk with average steady-state concentrations approximately 76% of those in maternal plasma. The estimated infant dose from breast milk (assuming mean milk consumption of 150 ml/kg/day) of women receiving 300 mg/day or the maximum dose of 600 mg/day would be 0.31 or 0.62 mg/kg/day, respectively. These estimated doses are approximately 7% of the total daily maternal dose on a mg/kg basis.

Pharmacotherapeutic group

The information provided in Pharmacotherapeutic group of Regapen is based on data of another medicine with exactly the same composition as the Regapen. . Be careful and be sure to specify the information on the section Pharmacotherapeutic group in the instructions to the drug Regapen directly from the package or from the pharmacist at the pharmacy.

Capsules; Substance; Substance-mixture; Substance-powder
Capsule, hard
Antiepileptics, other antiepileptics ATC code: N03AX16
Anti-epileptics, other anti-epileptics ATC code: N03AX16
Preclinical safety data

The information provided in Preclinical safety data of Regapen is based on data of another medicine with exactly the same composition as the Regapen. . Be careful and be sure to specify the information on the section Preclinical safety data in the instructions to the drug Regapen directly from the package or from the pharmacist at the pharmacy.

Capsules; Substance; Substance-mixture; Substance-powder
Capsule, hard

In conventional safety pharmacology studies in animals, Regapen was well-tolerated at clinically relevant doses. In repeated dose toxicity studies in rats and monkeys CNS effects were observed, including hypoactivity, hyperactivity and ataxia. An increased incidence of retinal atrophy commonly observed in aged albino rats was seen after long term exposure to Regapen at exposures > 5 times the mean human exposure at the maximum recommended clinical dose.

Regapen was not teratogenic in mice, rats or rabbits. Foetal toxicity in rats and rabbits occurred only at exposures sufficiently above human exposure. In prenatal/postnatal toxicity studies, Regapen induced offspring developmental toxicity in rats at exposures >2 times the maximum recommended human exposure.

Adverse effects on fertility in male and female rats were only observed at exposures sufficiently in excess of therapeutic exposure. Adverse effects on male reproductive organs and sperm parameters were reversible and occurred only at exposures sufficiently in excess of therapeutic exposure or were associated with spontaneous degenerative processes in male reproductive organs in the rat. Therefore the effects were considered of little or no clinical relevance.

Regapen is not genotoxic based on results of a battery of in vitro and in vivo tests.

Two-year carcinogenicity studies with Regapen were conducted in rats and mice. No tumours were observed in rats at exposures up to 24 times the mean human exposure at the maximum recommended clinical dose of 600 mg/day. In mice, no increased incidence of tumours was found at exposures similar to the mean human exposure, but an increased incidence of haemangiosarcoma was observed at higher exposures. The non-genotoxic mechanism of Regapen-induced tumour formation in mice involves platelet changes and associated endothelial cell proliferation. These platelet changes were not present in rats or in humans based on short term and limited long term clinical data. There is no evidence to suggest an associated risk to humans.

In juvenile rats the types of toxicity do not differ qualitatively from those observed in adult rats. However, juvenile rats are more sensitive. At therapeutic exposures, there was evidence of CNS clinical signs of hyperactivity and bruxism and some changes in growth (transient body weight gain suppression). Effects on the oestrus cycle were observed at 5-fold the human therapeutic exposure. Reduced acoustic startle response was observed in juvenile rats 1-2 weeks after exposure at >2 times the human therapeutic exposure. Nine weeks after exposure, this effect was no longer observable.

In conventional safety pharmacology studies in animals, pregabalin was well-tolerated at clinically relevant doses. In repeated dose toxicity studies in rats and monkeys CNS effects were observed, including hypoactivity, hyperactivity and ataxia. An increased incidence of retinal atrophy commonly observed in aged albino rats was seen after long-term exposure to pregabalin at exposures > 5 times the mean human exposure at the maximum recommended clinical dose.

Pregabalin was not teratogenic in mice, rats or rabbits. Foetal toxicity in rats and rabbits occurred only at exposures sufficiently above human exposure. In prenatal/postnatal toxicity studies, pregabalin induced offspring developmental toxicity in rats at exposures > 2 times the maximum recommended human exposure.

Pregabalin is not genotoxic based on results of a battery of in vitro and in vivo tests.

Two-year carcinogenicity studies with pregabalin were conducted in rats and mice. No tumours were observed in rats at exposures up to 24 times the mean human exposure at the maximum recommended clinical dose of 600 mg/day. In mice, no increased incidence of tumours was found at exposures similar to the mean human exposure, but an increased incidence of haemangiosarcoma was observed at higher exposures. The non-genotoxic mechanism of pregabalin-induced tumour formation in mice involves platelet changes and associated endothelial cell proliferation. These platelet changes were not present in rats or in humans based on short-term and limited long-term clinical data. There is no evidence to suggest an associated risk to humans.

In juvenile rats the types of toxicity do not differ qualitatively from those observed in adult rats. However, juvenile rats are more sensitive. At therapeutic exposures, there was evidence of CNS clinical signs of hyperactivity and bruxism and some changes in growth (transient body weight gain suppression). Effects on the oestrus cycle were observed at 5-fold the human therapeutic exposure. Reduced acoustic startle response was observed in juvenile rats 1-2 weeks after exposure at > 2 times the human therapeutic exposure. Nine weeks after exposure, this effect was no longer observable.

Incompatibilities

The information provided in Incompatibilities of Regapen is based on data of another medicine with exactly the same composition as the Regapen. . Be careful and be sure to specify the information on the section Incompatibilities in the instructions to the drug Regapen directly from the package or from the pharmacist at the pharmacy.

Toshkentda “Regapen” psixotrop dori vositasini noqonuniy sotgan dorixonachilarga nisbatan jinoiy ish qo‘zg‘atildi

Toshkent shahar IIBB jinoyat qidiruv boshqarmasi narkotik moddalarning noqonuniy aylanishiga qarshi kurashish bo‘limi xodimlari Bosh prokuratura huzuridagi Departament bilan hamkorlikda kuchli ta’sir etuvchi dori-darmonlarni noqonuniy sotadigan dorixonalar xodimlarini aniqlash maqsadida reyd o‘tkazdi, deb xabar berdi poytaxt IIBB matbuot xizmati.

Foto: Toshkent shahar IIBB matbuot xizmati

6-dekabr kuni Yakkasaroy tumani Usmon Nosir ko‘chasida joylashgan “Guli-kand plus” MChJ dorixonasi xodimlari 23 yoshli Sh.N va 29 yoshli Jasur.K maxsus retsept talab qilmasdan kuchli ta’sir qiluvchi “Regapen” preparatini sotayotgani aniqlandi. Bundan tashqari xodimlarning maxsus farmatsevtik ma’lumotga ega emasliklari ham aniqlangan.

Dorixona xodimlarini qo‘lga olishda maxsus kuchlar ishtirok etmagan.

Mazkur holat yuzasidan O‘zbekiston Respublikasi jinoyat kodeksining 251-1-moddasi (Kuchli ta’sir qiluvchi yoki zaharli moddalarni qonunga xilof ravishda egallash) bo‘yicha Sh.N. va J.K. ga nisbatan jinoiy ish qo‘zg‘atildi.

Foto: Toshkent shahar IIBB matbuot xizmati

Bundan tashqari, xuddi shunday jinoiy faoliyat holatlari Uchtepa tumanida joylashgan “Besh plus mega farm” MChJ dorixonasida ham aniqlanib, 658 dona “Regapen” dori vositasi ashyoviy dalil sifatida olingan.

Shuningdek, Chilonzor tumani 8-massivida joylashgan “Fayz farm” MChJ dorixonasidan ham 77 ta “Regapen” hamda 36 ta boshqa kuchli ta’sir qiluvchi dori preparatlarini musodara qilgan.

“Besh plus mega farm” va “Fayz farm” MChJ dorixonalari ishchilari 31 yoshli B.R. va 23 yoshli A.K.ga nisbatan O‘zbekiston Respublikasi jinoyat kodeksining 251-1-moddasi (Kuchli ta’sir qiluvchi yoki zaharli moddalarni qonunga xilof ravishda egallash) bo‘yicha jinoyat ishi qo‘zg‘atilgan.

Bu boradagi ishlar davom ettirilib, sodir etilgan qilmishlar uchun javobgarlikning muqarrarligi tamoyiliga rioya etilishi ta’minlanmoqda, deyiladi xabarda.

“Hurmatli hamshaharlar! Agar siz dorixona xodimi ‘Tropikamid’ yoki ‘Regapen’ dori vositasining retseptsiz yoki dorixonadan tashqarida sotilayotganiga guvoh bo‘lsangiz, 102 yoki 71-232-30-40, 71-232-40-50 telefon raqamlariga murojaat qilishingizni so‘raymiz. Ularga nisbatan qonun doirasida qat’iy choralar ko‘riladi” , — deyiladi xabarda.

Regapen qanday dori

Regapen qanday dori

Tarkibi:

Ta’sir etuvchi modda(XPN):

Preparatning savdo nomi:

Farmakalogik guruhi:

Dori shakli:

Regapen qanday dori

Toshkentda “Regapen” psixotrop dori vositasini noqonuniy sotgan dorixonachilarga nisbatan jinoiy ish qo‘zg‘atildi

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