Ammonium chloride Amphetamines

Phethenylate sodium Ammonium chloride Cyclofenil Methionine Ammonium sulfate Aminobenzoic acid Fibrinolysin Ammonium sulfamate Cyclamate calcium Ammonium thiocyanate Acetazolamide Clonidine HCl Tolonidine nitrate 2oxazo lamina d-Amphetamine Tanphetamin Ampicillin Mezlocillin Talampicillin... 

In addition to direct inhibition of the vesicular transport protein, storage of neurotransmitters can be reduced by dissipation of the proton electrochemical gradient. Bafilomycin (a specific inhibitor of the vacuolar H+-ATPase), as well as the proton ionophores carbonyl cyanide m-chlorophenylhydrazone (CCCP) and carbonylcyanide p-(trifluoromethoxy) phenylhy-drazone (FCCP) are used experimentally to reduce the vesicular storage of neurotransmitters. Weak bases including amphetamines and ammonium chloride are used to selectively reduce ApH. 

The risk of tachycardia, hypertension, and cardiotoxicity is increased with coadministration of dronabinol (an antiemetic) and dextroamphetamine. In addition, administration of dextroamphetamine with MAOIs may increase the risk of hypertensive crisis. Al-kalinizing agents can speed absorption (e.g., antacids) or delay urinary excretion (e.g., acetazolamide, thiazide diuretics) of dextroamphetamine, thus potentiating its effects. Gastric or urinary acidifying agents (e.g., ascorbic acid, ammonium chloride) can decrease the effects of dextroamphetamine. Propoxyphene overdose can potentiate amphetamine central nervous system stimulation, potentially resulting in fatal convulsions. 

Ammonium chloride increases urinary volume with acidification of urine. The excretion of amphetamine is decreased in relatively alkaline urine and has proved useful in the treatment of amphetamine intoxication. ... 

Nonionized lipid-soluble drugs are resorbed and not eliminated. Generally, drugs that are bases are excreted when the urine is acidic, whereas acidic compounds are excreted in greater quantities if the urine is alkaline. For example, in phenobarbital (weak acid pKa of 7.3) poisoning, alkalinization of the urine with sodium bicarbonate is helpful in eliminating the phenobarbital. In amphetamine toxicity, acidification of the urine with ammonium chloride is required (Figure 1.13). 

Frequent symptoms of amphetamine withdrawal include excessive fatigue and depression. These may also occur nausea, vomiting, chills, cramps, headaches, and arrhythmia (a change in the rhythm of the heartbeat). A physician may prescribe antidepressants to help alleviate depression during amphetamine withdrawal. Also during withdrawal, if psychosis and/or hallucinations are experienced, treatment with chlorpromazine (Thorazine) or haloperidol (Haldol) may be necessary. Finally, ammonium chloride may be prescribed to more quickly remove amphetamines through the urine. 

Sometimes, we may want to use a f-test in a way that differs from our previous approach. Say, for example, we are considering the use of urinary acidification to hasten the clearance of amphetamine from patients who have overdosed. An initial trial in rabbits is used to test the general principal. One group of rabbits receives ammonium chloride to induce a lower urinary pH and another group acts as controls. All rabbits receive a test dose of radio-labelled drug, the clearance of which is studied over a few hours. In this case, the question posed should be is there an increase in clearance rather than the standard is there a difference in clearance The former constitutes a one-sided question. 

Acidification may be used for severe, acute amphetamine, dexfenfluramine or phencyclidine poisoning. The objective is to maintain a urine pH of 5.5-65 by giving i.v. infusion of arginine hydrochloride (10 g) over 30 min, followed by ammonium chloride (4 g) 2-hourly by mouth. It is rarely necessary. Phenoxybenzamine should be adequate for amphetamine-like drugs (a-adrenoceptor block). 

Renal excretion of basic drugs such as amphetamine theoretically can be enhanced by acidification of the urine. Acidification can be accomplished by the administration of ammonium chloride or ascorbic acid. Urinary excretion of an acidic compound is particularly sensitive to changes in urinary pH if its is within the range of 3.0-7.5 for bases, the corresponding pH range is 7.5-10.5. 

The use of platinum as the catalyst in the bomb works great when making MDMA, but gives lousy results when making MDA. There may be a way around this, however, for serious experimenters. It has been found in experiments with phenylacetone that a mixture of ammonia and ammonium chloride produces good yields of amphetamine (50%) when used in a bomb with platinum catalyst. Methylenedioxyphenylacetone is quite likely to behave similarly, along with other phenylacetones. 

A closely related 2C-T-X compound was also started quite a while later -this was the allylthio homologue of the methallyl material 2C-T-3 or 2C-T-20. Its place in the flow of things is evident from its numbering, 2C-T-16. A mixture of 2,5-dimethoxythiophenol and KOH and allyl chloride in MeOH gave 2,5-dimethoxyphenyl allyl sulfide as a white oil which boiled at 110-125 °C at 0.25 mm/Hg. This, with POCI3 and N-methylformanilide provided 2,5-dimethoxy-4-(allylthio)benzaldehyde which distilled at 140-160 °C at 0.4 mm/Hg and could be recrystallized from MeOH as a pale yellow solid. Reaction of this aldehyde in nitroethane in the presence of ammonium acetate (steam bath for 2.5 h) provided 2,5-dimethoxy-4-allylthio-beta-nitrostyrene as red crystals from acetonitrile. Its mp was 114-115 °C. Anal. (C13H15N04S) C,H. This has not yet been reduced to the final amine, 2,5-dimethoxy-4-allylthiophenethylamine, 2C-T-16. The corresponding amphetamine would be, of course, ALEPH-16. 

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