Author Topic: chloropseudoephedrine potency  (Read 2876 times)

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masterofpuppets

  • Guest
chloropseudoephedrine potency
« on: August 09, 2001, 11:17:00 PM »
Hey, does anyone know whether munching on some chloroephedrine would do anything?  How potent is it (I have heard that it can make all u male bees impotent, although that might just be a rumour)?  Thanks for any info.

Everyone repeat after me - "I am an individual, just like everybody else"

Rhodium

  • Guest
Re: chloropseudoephedrine potency
« Reply #1 on: August 10, 2001, 07:53:00 AM »
As far as I know, it is not psychoactive, but has a lot of peripheral side effects.

monkpea

  • Guest
Re: chloropseudoephedrine potency
« Reply #2 on: August 10, 2001, 05:14:00 PM »
What about esters and ethers of ephedrine and pseudoephedrine?

I thought the problem lay with the OH inhibiting passage across the blood brain barrier. If ketones can get through (methcathinone) then perhaps the methyl ether or formic ester might be of interest?

Rhodium

  • Guest
Re: chloropseudoephedrine potency
« Reply #3 on: August 10, 2001, 07:49:00 PM »
The methyl ether should be active (look at the BOX series of compounds in Pihkal), but I guess the ester would hydrolyze pretty quickly in the body.

Tengo

  • Guest
What kind of side effects would you expect?
« Reply #4 on: December 10, 2002, 02:33:00 AM »
What kind of side effects would you expect?

Rhodium

  • Guest
Increased heart rate and blood pressure, coldness ...
« Reply #5 on: December 11, 2002, 12:26:00 AM »
Increased heart rate and blood pressure, coldness in the limbs due to blood vessels constricting, shallow breathing/tightness over the chest etc... Not fun. PMA and PMMA often gives these effects too.

dwarfer

  • Guest
chloro pseudo and ehedrine
« Reply #6 on: December 11, 2002, 12:51:00 PM »
Are they not both a yellow tint?

Wouldn't they be distiguishable against the white-white
of meth?

dwarfer

Rhodium

  • Guest
The hydrochloride salts of both (pseudo)ephedrine ...
« Reply #7 on: December 11, 2002, 06:35:00 PM »
The hydrochloride salts of both (pseudo)ephedrine and chloro(pseudo)ephedrine should be perfectly white, if not - they are impure.

12345x

  • Guest
a friend of mine....
« Reply #8 on: December 22, 2002, 08:09:00 AM »
one time long ago
i was making shit via chloroephedrine
and had just finished cleaning up the chloro
and was preparing the pall.acetate water.
when a friend of mine agenst my wishes
tryed some of those preaty yellow tinted crystals.
and he after sticking some in his arm
said he didnt feel anything.
but he also said that he got a chlorine taist in his mouth.


so go figger.

Rhodium

  • Guest
Toxicity of chloropseudoephedrine/chloroephedrine
« Reply #9 on: December 25, 2002, 02:45:00 PM »
Here you go - pharmacology and toxicity of chloro(pseudo)ephedrine (same as "chloromethamphetamine"):

Chloroephedrine: Contaminant of methamphetamine synthesis with cardiovascular activity
Kurt J. Varner, Nichole D. Hein, Brian A. Ogden, Jody R. Arsenault, Karen M. Carter, William H. Soine

Drug and Alcohol Dependence 64, 299–307 (2001)

(https://www.thevespiary.org/rhodium/Rhodium/pdf/chloroephedrine.pdf)

Abstract
Chloroephedrine is an intermediate and possible contaminant formed when methamphetamine is manufactured using ephedrine or pseudoephedrine as precursors. The purpose of this study was to determine whether this contaminant has biological activity and might contribute to methamphetamine-induced cardiovascular toxicity. In conscious rats, the (?) and (+) isomers of chloroephedrine (0.1 and 1.0 mg/kg, i.v.) dose-dependently increased mean arterial pressure (MAP) and heart rate (HR). The potency of the pressor effects of (?) and (+)-chloroephedrine was between that of ephedrine and pseudoephedrine. The increases in HR elicited by the four stimulants were similar except that the tachycardia elicited by all doses of ephedrine and pseudoephedrine were preceded by a brief decrease in HR. The i.v. administration of 10 mg/kg of (+) or (?)-chloroephedrine produced biphasic (decrease followed by increase) the MAP and HR responses. Ephedrine and pseudoephedrine did not decrease MAP at any dose tested. The initial decrease in HR elicited by (?)-chloroephedrine was significantly reduced and the hypotensive response abolished by atropine, indicating that these components of the MAP and HR responses resulted from vagal activation. The secondary pressor response elicited by (?)-chloroephedrine was significantly reduced and the tachycardia significantly increased by pretreatment with phentolamine (3 mg/kg, i.v.). The increase in HR was reversed by propranolol. These results indicate that (?) and (+)-chloroephedrine have sympathomimetic properties similar to other known sympathomimetic stimulants. In addition, larger doses of chloroephedrine can activate the vagus nerve. The combination of (+)-methamphetamine and (?)-chloroephedrine did not markedly alter the magnitude of the MAP and HR responses of (+)-methamphetamine alone except at high doses of (?)-chloroephedrine (10 mg/kg). Contamination of illicit methamphetamine with chloroephedrine may have toxic consequences.

Rhodium

  • Guest
Chloroephedrine Irreversible CYP2D6 Inhibition
« Reply #10 on: March 31, 2004, 08:26:00 AM »
Irreversible Inhibition of CYP2D6 by (-)-Chloroephedrine, a Possible Impurity in Methamphetamine
B. Rege, K. M. Carter, M. A. Sarkar, G. E. Kellogg, and W. H. Soine

Drug. Metab. Disp. 30(12), 1337-1343 (2002)

(http://dmd.aspetjournals.org/cgi/content/full/30/12/1337)

Abstract
(+)- and (-)-Chloroephedrine, and their respective aziridines, cis- and trans-1,2-dimethyl-3-phenylaziridine, have been reported present in clandestinely synthesized methamphetamine. Since methamphetamine and structurally related compounds are potential substrates for human liver CYP2D6, the possible interaction of the chloroephedrines with human liver CYP2D6 was evaluated. Computational methods (using Flexidock and HINT in SYBYL) were used to determine the feasibility of (+)- or (-)-chloroephedrine and cis- or trans-1,2-dimethyl-3-phenylaziridine binding in the active site of a three dimensional CYP2D6 molecular model. Although modeling indicates both (+)- and (-)-chloroephedrine would bind comparably to methamphetamine, the binding energies of cis- or trans-1,2-dimethyl-3-phenylaziridine products indicate a preference for trans-1,2-dimethyl-3-phenylaziridine, the product formed from (-)-chloroephedrine. The effects of (+)- and (-)-chloroephedrine on the metabolism of dextromethorphan in human liver microsomes were then experimentally evaluated. (+)-Chloroephedrine (50 µM) had no effect on human CYP2D6. (-)-Chloroephedrine appeared to be selective for human CYP2D6 versus CYP1A2 and CYP3A4/5. The inhibition of CYP2D6 was time-dependent, not dependent on metabolic activation, and irreversible. It appeared to bind at the active site of CYP2D6 with an apparent Ki of 226 µM, with a kint of 0.039 min1, and a t1/2 of 23 min. Due to the irreversible nature of this inhibition, this impurity in clandestinely synthesized methamphetamine may be important and warrant further study.