Diclazepam Pills: Diclazepam (Ro5-3448), also known as chlorodiazepam and 2′-chloro-diazepam, is a benzodiazepine and functional analog of diazepam. It was first synthesized by Leo Sternbach and his team at Hoffman-La Roche in 1960. It is not currently approved for use as a medication, but rather sold as an unscheduled substance. Efficacy and safety have not been tested in humans. In animal models, its effects are similar to diazepam, possessing long-acting anxiolytic, anticonvulsant, hypnotic, sedative, skeletal muscle relaxant, and amnestic properties
Diclazepam is a drug of the benzodiazepine class. Benzodiazepine drugs contain a benzene ring fused to a diazepine ring, which is a seven-membered ring with the two nitrogen constituents located at R1 and R4. At R1, diclazepam is substituted with methyl group. Further, the benzodiazepine ring is bonded at R5 to a 2-chlorinated phenyl ring. R7 of the benzyl ring is also substituted with a chlorine group. Diclazepam also contains an oxygen group double bonded to R2 of its diazepine ring to form a ketone. This oxygen substitution at R2 is shared with other benzodiazepine drugs with the suffix -azepam.
Metabolism of this compound has been assessed, revealing diclazepam has an approximate elimination half-life of 42 hours and undergoes N-demethylation to delorazepam, which can be detected in urine for 6 days following administration of the parent compound. Other metabolites detected were lorazepam and lormetazepam which were detectable in urine for 19 and 11 days, respectively, indicating hydroxylation by cytochrome P450 enzymes occurring concurrently with N-demethylation.
Benzodiazepines produce a variety of effects by binding to the benzodiazepine receptor site and magnifying the efficiency and effects of the neurotransmitter gamma aminobutyric acid (GABA) by acting on its receptors. As this site is the most prolific inhibitory receptor set within the brain, its modulation results in the sedating (or calming effects) of diclazepam on the nervous system.
Diclazepam has an approximate elimination half-life of 42 hours and undergoes N-demethylation to delorazepam, which can be detected in urine for 6 days following administration of the parent compound. Other metabolites detected were lorazepam and lormetazepam which were detectable in urine for 19 and 11 days, respectively, indicating hydroxylation by cytochrome P450 enzymes occurring concurrently with N-demethylation.
The anticonvulsant properties of benzodiazepines may be, in part or entirely, due to binding to voltage-dependent sodium channels rather than benzodiazepine receptors.
Disclaimer: The effects listed below cite the Subjective Effect Index (SEI), an open research literature based on anecdotal user reports and the personal analyses of PsychonautWiki contributors. As a result, they should be viewed with a healthy degree of skepticism.
It is also worth noting that these effects will not necessarily occur in a predictable or reliable manner, although higher doses are more liable to induce the full spectrum of effects. Likewise, adverse effects become increasingly likely with higher doses and may include addiction, severe injury, or death
- Muscle relaxation
- Sedation – In terms of energy level alterations, this drug has the potential to be extremely sedating and often results in an overwhelmingly lethargic state. At higher levels, this causes users to suddenly feel as if they are extremely sleep deprived and have not slept for days, forcing them to sit down and generally feel as if they are constantly on the verge of passing out instead of engaging in physical activities. This sense of sleep deprivation increases proportional to dosage and eventually becomes powerful enough to force a person into complete unconsciousness.
- Motor control loss
- Respiratory depression
- Paradoxical reactions to benzodiazepines such as increased seizures (in epileptics), aggression, increased anxiety, violent behavior, loss of impulse control, irritability and suicidal behavior sometimes occur (although they are rare in the general population, with an incidence rate below 1%).These paradoxical effects occur with greater frequency in recreational abusers, individuals with mental disorders, children, and patients on high-dosage regimes.
- The cognitive effects of diclazepam can be broken down into several components which progressively intensify proportional to dosage. The general head space of diclazepam is described by many as one of intense sedation and decreased inhibition. It contains a large number of typical depressants cognitive effects. The most prominent of these cognitive effects generally include:
- Anxiety suppression
- Thought deceleration
- Analysis suppression
- Compulsive redosing
- Emotion suppression – Although this compound primarily suppresses anxiety, it also dulls other emotions in a manner which is distinct but less intensive than that of antipsychotics.
- Delusions of sobriety – This is the false belief that one is perfectly sober despite obvious evidence to the contrary such as severe cognitive impairment and an inability to fully communicate with others. It most commonly occurs at heavy dosages.
- Dream potentiation
- Rebound anxiety – Rebound anxiety is a commonly observed effect with anxiety relieving substances like benzodiazepines. It typically corresponds to the total duration spent under the substance’s influence along with the total amount consumed in a given period, an effect which can easily lend itself to cycles of dependence and addiction.
- Dream potentiation or Dream suppression
- Residual sleepiness – While benzodiazepines can be used as an effective sleep-inducing aid, their effects may persist into the morning afterward, which may lead users to feeling “groggy” or “dull” for up to a few hours.
- Thought deceleration
- Thought disorganization