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Downers and sleeping pills Anxiety Meds, Sleeping Pills and Skeletal Muscle Relaxants

 
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  #1  
Old 23-02-2006, 10:26
rideburton56 rideburton56 is offline
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sonota (Zaleplon) is amazing

i have these meds prescribed to me and I decided today would be a good experimenttation. SONOTA 10 comes in a blugreen/nave blue tabs that are very easy to break apart. (already fluffy) this morning swim ha smoked 4 bowls, blow 1omg adderall XL to wake up, smoked again, ate dinner and started. i decided i was gonna try and practice sniffing hte pill withoutmaking it obvious like just a odd gesture. which i came up with but it took like 4 pills, and blew two pills with my boy so he try it. Initially hwen u do a line, when ur head come up or u walk around a lot u get real dissy and this drugs brings down your mototskills a lot overall. hugeeeeeee eurphoria, so relaxed i cant even more, absolutely 100% visuals for esxample this whole trip has been in the water and as i type im looking through a pool and on the see floor is the screen to type. there type of shift in color as well, like almost a purple to yellow fade diagnol. dont overuse, cuz if u stich to doing it once a week around there, its ok to take one just for fun
  #2  
Old 23-02-2006, 20:59
Jatelka Jatelka is offline
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Sonata Pharma Info

Sonata is zaleplon.

It is a nonbenzodiazepine hypnotic from the pyrazolopyrimidine class. The chemical name of zaleplon is N-[3-(3-cyanopyrazolo[1,5-a]pyrimidin-7-yl)phenyl]-N-ethylacetamide. Its empirical formula is C17H15N5O, and its molecular weight is 305.34.

It is a white to off-white powder that is practically insoluble in water and sparingly soluble in alcohol or propylene glycol. Its partition coefficient in octanol/water is constant (log PC = 1.23) over the pH range of 1 to 7.

Inactive ingredients of Sonata capsules consist of microcrystalline cellulose, pregelatinized starch, silicon dioxide, sodium lauryl sulfate, magnesium stearate, lactose, gelatin, titanium dioxide, D&C yellow #10, FD&C blue #1, FD&C green #3, and FD&C yellow #5.

It interacts with the gamma-aminobutyric acid-benzodiazepine (GABA-BZ) receptor complex. Subunit modulation of the GABA-BZ receptor chloride channel macromolecular complex is hypothesized to be responsible for some of the pharmacological properties of benzodiazepines, which include sedative, anxiolytic, muscle relaxant, and anticonvulsive effects in animal models.

Other nonclinical studies have also shown that zaleplon binds selectively to the brain omega-1 receptor situated on the alpha subunit of the GABAA/chloride ion channel receptor complex and potentiates t-butyl-bicyclophosphorothionate (TBPS) binding. Studies of binding of zaleplon to recombinant GABAA receptors (a1b1g2 [omega-1] and a2b1g2 [omega-2]) have shown that zaleplon has a low affinity for these receptors, with preferential binding to the omega-1 receptor.

It is rapidly absorbed with a time to peak concentration of approximately 1 hour and a half-life of approximately 1 hour. It does not accumulate with once-daily administration and its pharmacokinetics are dose proportional in the therapeutic range.

It is rapidly and almost completely absorbed following oral administration. Peak plasma concentrations are attained within approximately 1 hour after oral administration. Although zaleplon is well absorbed, its absolute bioavailability is approximately 30% because it undergoes significant presystemic metabolism.

It is a lipophilic compound with a volume of distribution of approximately 1.4 L/kg following intravenous (IV) administration, indicating substantial distribution into extravascular tissues. The in vitro plasma protein binding is approximately 60%±15% and is independent of zaleplon concentration over the range of 10 ng/mL to 1000 ng/mL. This suggests that zaleplon disposition should not be sensitive to alterations in protein binding. The blood to plasma ratio for zaleplon is approximately 1, indicating that zaleplon is uniformly distributed throughout the blood with no extensive distribution into red blood cells.

After oral administration, it is extensively metabolized, with less than 1% of the dose excreted unchanged in urine. Zaleplon is primarily metabolized by aldehyde oxidase to form 5-oxo-zaleplon. Zaleplon is metabolized to a lesser extent by cytochrome P450 (CYP) 3A4 to form desethylzaleplon, which is quickly converted, presumably by aldehyde oxidase, to 5-oxo-desethylzaleplon. These oxidative metabolites are then converted to glucuronides and eliminated in urine. All of zaleplon’s metabolites are pharmacologically inactive.

After either oral or IV administration, is rapidly eliminated with a mean half life of of approximately 1 hour. The oral-dose plasma clearance of zaleplon is about 3 L/h/kg and the IV zaleplon plasma clearance is approximately 1 L/h/kg. It is subject to high first pass metabolism by the liver.

It is metabolized primarily by the liver and undergoes significant presystemic metabolism. Consequently, the clearance of zaleplon was reduced by 70%and 87% in compensated and decompensated cirrhotic patients, respectively, leading to marked increases in plasma concentration in comparison with healthy subjects. The dose of Sonata should therefore be reduced in patients with mild to moderate hepatic impairment. Sonata is not recommended for use in patients with severe hepatic impairment.

Renal impairment: Because renal excretion of unchanged zaleplon accounts for less than 1% of the administered dose, the pharmacokinetics of zaleplon are not altered in patients with renal insufficiency. No dose adjustment is necessary in patients with mild to moderate renal impairment. Sonata has not been adequately studied in patients with severe renal impairment.

Sonata is indicated for the short term treatment of insomnia. It reduces the time to sleep onset for up to 30 days (controlled studies). It has not been shown to increase sleep time or to reduce the number of awakenings.

Recommended dose of Sonata for most nonelderly adults is 10 mg. For certain low weight individuals, 5 mg may be a sufficient dose. Although the risk of certain adverse events associated with the use of Sonata appears to be dose dependent, the 20 mg dose has been shown to be adequately tolerated and may be considered for the occasional patient who does not benefit from a trial of a lower dose. Doses above 20 mg have not been adequately evaluated and are not recommended.

Sonata capsules are available in bottles of 100 capsules in the following dosage strengths:

5 mg, NDC 0008-0925, opaque green cap and opaque pale green body with "5 mg" on the cap and "SONATA" on the body.

10 mg, NDC 0008-0926, opaque green cap and opaque light green body with "10 mg" on the cap and "SONATA" on the body.

Adverse effects include: Abdominal pain, altered sensation, fatigue/malaise, photosensitivity, anorexia, nausea, diarrhoea, oedema, confusion, depersonalization, dizziness, hallucinations, drowsiness, tremor, vertigo, blurred vision, painful/heavy periods, headache/migraine and hangover effect, myalgia, arthralgia, anxiety (including rebound), increased sputum production

Infrequently: Angina, hypertension, cardiac arryhthmias, gastritis, mouth ulceration, diabetes, hypothyroidism, anaemia, gout, raised blood lipids, ataxia, lowered libido, exacerbation of asthma, and anaphylaxis

Sonata is a schedule IV substance in the US (as far as SWIM aware not available in UK)

Two studies have assessed the abuse liability of Sonata at doses of 25 mg, 50 mg, and 75 mg in subjects with known histories of sedative drug abuse. The results of these studies indicate that Sonata has an abuse potential similar to benzodiazepine and benzodiazepine-like hypnotics.

The potential for developing physical dependence on Sonata and a subsequent withdrawal syndrome has been assessed in controlled studies. Some patients (mostly those treated with 20 mg) experienced a mild rebound insomnia on the first night that appears to resolve quickly.

There is no other current evidence regarding a withdrawal syndrome, however seizures and death have been observed in animal studies with withdrawal of high dose Sonata.

Sonata is contrindicated in those with a history of drug or alcohol dependance.

Tolerance to Sonata quickly develops at doses of 10mg and 20mg.

Sonata has an additive effect with alcohol, benzodiazepines, and tricyclics, but not SSRI's. Drugs which induce hepatic enzymes are likely to reduce efficacy. Hepatic enzyme inhibitors increase plasma concentrations.

In overdose: Central nervous system depression ranging from drowsiness to coma. In mild cases, confusion, and lethargy; in more serious cases, symptoms may include ataxia, hypotonia, hypotension, respiratory depression, rarely coma, and very rarely death.

(with thanks to rxlist)
  #3  
Old 23-02-2006, 21:10
Micklemouse Micklemouse is offline
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Zaleplon is indeed available in Briton...

From BNF 50

ZALEPLON



Indications:

insomnia (short-term use—up to 2 weeks)

Cautions:

respiratory insufficiency (avoid if severe); hepatic impairment (avoid if severe; ; history of drug or alcohol abuse; avoid prolonged use (and abrupt withdrawal thereafter); pregnancy ; not for use alone to treat depression

Contra-indications:

sleep apnoea syndrome, myasthenia gravis; not for use alone to treat psychosis; breast-feeding

Side-effects:

amnesia, paraesthesia, drowsiness, asthenia; nausea, incoordination, confusion, impaired concentration, dizziness, hallucinations, disturbances of hearing, smell, speech, and vision, photosensitivity; dependence; paradoxical effects (discontinue)

Dose:

10 mg at bedtime or after going to bed if difficulty falling asleep; elderly 5 mg; child under 18 years not recommended
Note

. Patients should be advised not to take a second dose during a single night




Zaleplon


Zaleplon has the following interaction information:
Cimetidine-metabolism of zaleplon inhibited by cimetidine (increased plasma concentration)



Rifampicin-metabolism of zaleplon possibly accelerated by rifampicin

Zaleplon belongs to Anxiolytics and Hypnotics and will have the following interactions:
ACE Inhibitors -enhanced hypotensive effect when anxiolytics and hypnotics given with ACE inhibitors

Adrenergic Neurone Blockers - enhanced hypotensive effect when anxiolytics and hypnotics given with adrenergic neurone blockers

Alcohol increased sedative effect when anxiolytics and hypnotics given with alcohol

Alpha Blockers enhanced hypotensive and sedative effects when anxiolytics and hypnotics given with alpha-blockers

Anaesthetics, General increased sedative effect when anxiolytics and hypnotics given with general anaesthetics See also Surgery and Long-term Medication,

Angiotensin-II Receptor Agonists enhanced hypotensive effect when anxiolytics and hypnotics given with angiotensin-II receptor antagonists

Antidepressants, Tricyclic increased sedative effect when anxiolytics and hypnotics given with tricyclics

Antidepressants,Tricyclic (related) increased sedative effect when anxiolytics and hypnotics given with tricyclic-related antidepressants

Antihistamines increased sedative effect when anxiolytics and hypnotics given with antihistamines Sedative interactions apply to a lesser extent to the non-sedating antihistamines. Interactions do not generally apply to antihistamines used for topical action (including inhalation)

Antipsychotics increased sedative effect when anxiolytics and hypnotics given with antipsychotics Increased risk of toxicity with myelosuppressive drugs

Baclofen increased sedative effect when anxiolytics and hypnotics given with Baclofen

BetaBlockers enhanced hypotensive effect when anxiolytics and hypnotics given with beta-blockers Since systemic absorption may follow topical application of beta-blockers to the eye the possibility of interactions, in particular, with drugs such as verapamil should be borne in mind

Calcium Channel Blockers enhanced hypotensive effect when anxiolytics and hypnotics given with calcium-channel blockers Dihydropyridine calcium-channel blockers include amlodipine, felodipine, isradipine, lacidipine, lercanidipine, nicardipine, nifedipine, nimodipine, and nisoldipine

Clonidine enhanced hypotensive effect when anxiolytics and hypnotics given with clonidine

Diazoxide enhanced hypotensive effect when anxiolytics and hypnotics given with diazoxide

Diuretics enhanced hypotensive effect when anxiolytics and hypnotics given with diuretics

Hydralazine enhanced hypotensive effect when anxiolytics and hypnotics given with hydralazine

Lofexidine increased sedative effect when anxiolytics and hypnotics given with lofexidine

Methyldopa enhanced hypotensive effect when anxiolytics and hypnotics given with methyldopa

Minoxidil enhanced hypotensive effect when anxiolytics and hypnotics given with minoxidil

Mirtazapine increased sedative effect when anxiolytics and hypnotics given with mirtazapine

Moxonidine enhanced hypotensive effect when anxiolytics and hypnotics given with moxonidine

Nabilone increased sedative effect when anxiolytics and hypnotics given with nabilone

Nitrates enhanced hypotensive effect when anxiolytics and hypnotics given with nitrates

Nitroprusside enhanced hypotensive effect when anxiolytics and hypnotics given with nitroprusside

Opioid analgesics increased sedative effect when anxiolytics and hypnotics given with opioid analgesics

Ritonavir plasma concentration of anxiolytics and hypnotics possibly increased by ritonavir

Tizanidine increased sedative effect when anxiolytics and hypnotics given with tizanidine


(Apologies to the boys and girls at the BNF if I've broken copyright by lifting this!)

Last edited by Micklemouse; 24-02-2006 at 00:13.
  #4  
Old 24-02-2006, 03:57
rideburton56 rideburton56 is offline
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wow i dont remember making that post last night.. sorry to all who tried to stumble through that awful trip report

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