Cocaine | CAS:50-36-2 | Manufacturer ChemFaces

Cocaine

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Description:

Cocaine is a powerfully addictive stimulant drug made from the leaves of the coca plant native to South America, it produces short-term euphoria. Cocaine has a small number of accepted medical uses such as numbing and decreasing bleeding during nasal surgery, it constricts blood vessels, dilates pupils, and increases body temperature, heart rate, and blood pressure. Cocaine sensitizes VTA cells to the excitatory effects of both CRF and orexin-A, thus providing a mechanism by which stress induces Cocaine seeking.Cocaine also can cause headaches and gastrointestinal complications such as abdominal pain and nausea. Because cocaine tends to decrease appetite, chronic users can become malnourished as well.

Targets:

NMDAR | HIV | gp120/CD4

In vivo:

Psychiatry Res. 2015 Feb 28;225(3):309-14.

Changes in brain-derived neurotrophic factor (BDNF) during abstinence could be associated with relapse in cocaine-dependent patients.[Pubmed: 25592977 ]

Brain-derived neurotrophic factor (BDNF) is involved in Cocaine craving in humans and drug seeking in rodents. Based on this, the aim of this study was to explore the possible role of serum BDNF in Cocaine relapse in abstinent addicts.
METHODS AND RESULTS:
Forty Cocaine dependent subjects (DSM-IV criteria) were included in an inpatient 2 weeks abstinence program. Organic and psychiatric co-morbidities were excluded. Two serum samples were collected for each subject at baseline and at after 14 abstinence days. After discharge, all Cocaine addicts underwent a 22 weeks follow-up, after which they were classified into early relapsers (ER) (resumed during the first 14 days after discharge,) or late relapsers (LR) (resumed beyond 14 days after discharge). The only clinical differences between groups were the number of consumption days during the last month before detoxification. Serum BDNF levels increased significantly across the 12 days of abstinence in the LR group (p=0.02), whereas in the ER group BDNF remained unchanged. In the ER group, the change of serum BDNF during abstinence negatively correlated with the improvement in depressive symptoms (p=0.02).
CONCLUSIONS:
These results suggest that BDNF has a role in relapse to Cocaine consumption in abstinent addicts, although the underlying neurobiological mechanisms remain to be clarified.

South Med J. 2015 Feb;108(2):130-1.

Effects of cocaine-positive urine screens on serum thyrotropin levels in patients admitted to an inpatient mental health unit.[Pubmed: 25688900]

To assess the effect of a positive urine screen for Cocaine on thyrotropin (TSH, also thyroid-stimulating hormone) concentrations.
METHODS AND RESULTS:
In this retrospective cohort study, patients admitted to the mental health unit at an academic inpatient setting with a diagnosis of Cocaine dependence or Cocaine intoxication were routinely screened with urine drug toxicology tests and TSH concentrations. TSH concentrations from patients who tested positive for Cocaine on urine toxicology were compared with patients having negative Cocaine screenings. A total of 192 patients were included: 122 with a positive Cocaine screen and 70 with a negative Cocaine screen. All patients were screened using a highly sensitive TSH assay. A positive Cocaine screen was not associated with a statistically significant difference in TSH concentrations compared with a negative Cocaine screen. The percentage of patients with hypothyroidism (TSH >4.50 μIU/mL) or hyperthyroidism (TSH <0.40 μIU/mL) were similar in both study groups.
CONCLUSIONS:
The study failed to show that a positive urine screen for Cocaine was associated with a significant effect on serum TSH levels in patients admitted to a mental health unit with a diagnosis of Cocaine dependence or Cocaine intoxication. Our findings support those of a prior study that Cocaine use does not affect routine thyroid function tests. The present study does not support the clinical practice of ordering a serum TSH screening test on patients admitted to inpatient psychiatry units soley because the urine screen is positive for Cocaine.

Cocaine Description

Source:	The leaves of the coca plant.
Solvent:	Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
Storage:	Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C). Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour. Need more advice on solubility, usage and handling? Please email to: service@chemfaces.com
After receiving:	The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.

Kinase Assay:

J Neurosci. 2015 Apr 29;35(17):6639-53.

Orexin-corticotropin-releasing factor receptor heteromers in the ventral tegmental area as targets for cocaine.[Pubmed: 25926444]

Release of the neuropeptides corticotropin-releasing factor (CRF) and orexin-A in the ventral tegmental area (VTA) play an important role in stress-induced Cocaine-seeking behavior.
METHODS AND RESULTS:
We provide evidence for pharmacologically significant interactions between CRF and orexin-A that depend on oligomerization of CRF1 receptor (CRF1R) and orexin OX1 receptors (OX1R). CRF1R-OX1R heteromers are the conduits of a negative crosstalk between orexin-A and CRF as demonstrated in transfected cells and rat VTA, in which they significantly modulate dendritic dopamine release. The Cocaine target σ1 receptor (σ1R) also associates with the CRF1R-OX1R heteromer. Cocaine binding to the σ1R-CRF1R-OX1R complex promotes a long-term disruption of the orexin-A-CRF negative crosstalk.
CONCLUSIONS:
Through this mechanism, Cocaine sensitizes VTA cells to the excitatory effects of both CRF and orexin-A, thus providing a mechanism by which stress induces Cocaine seeking.

Cell Research:

J Leukoc Biol. 2015 Apr;97(4):779-90.

Cocaine modulates HIV-1 integration in primary CD4+ T cells: implications in HIV-1 pathogenesis in drug-abusing patients.[Pubmed: 25691383]

Epidemiologic studies suggest that Cocaine abuse worsens HIV-1 disease progression. Increased viral load has been suggested to play a key role for the accelerated HIV disease among Cocaine-abusing patients. The goal of this study was to investigate whether Cocaine enhances proviral DNA integration as a mechanism to increase viral load.
METHODS AND RESULTS:
We infected CD4(+) T cells that are the primary targets of HIV-1 in vivo and treated the cells with physiologically relevant concentrations of Cocaine (1 µM-100 µM). Proviral DNA integration in the host genome was measured by nested qPCR. Our results illustrated that Cocaine from 1 µM through 50 µM increased HIV-1 integration in CD4(+) T cells in a dose-dependent manner. As integration can be modulated by several early postentry steps of HIV-1 infection, we examined the direct effects of Cocaine on viral integration by in vitro integration assays by use of HIV-1 PICs. Our data illustrated that Cocaine directly increases viral DNA integration. Furthermore, our MS analysis showed that Cocaine is able to enter CD4(+) T cells and localize to the nucleus-.
CONCLUSIONS:
In summary, our data provide strong evidence that Cocaine can increase HIV-1 integration in CD4(+) T cells. Therefore, we hypothesize that increased HIV-1 integration is a novel mechanism by which Cocaine enhances viral load and worsens disease progression in drug-abusing HIV-1 patients.

Animal Research:

J Pharmacol Exp Ther. 2015 Jun;353(3):465-70.

Availability of N-Methyl-d-Aspartate Receptor Coagonists Affects Cocaine-Induced Conditioned Place Preference and Locomotor Sensitization: Implications for Comorbid Schizophrenia and Substance Abuse.[Pubmed: 25788713]

Schizophrenia is associated with high prevalence of substance abuse. Recent research suggests that dysregulation of N-methyl-d-aspartate receptor (NMDAR) function may play a role in the pathophysiology of both schizophrenia and drug addiction, and thus, may account for this high comorbidity.
METHODS AND RESULTS:
Our laboratory has developed two transgenic mouse lines that exhibit contrasting NMDAR activity based on the availability of the glycine modulatory site (GMS) agonists d-serine and glycine. Glycine transporter 1 knockdowns (GlyT1(+/-)) exhibit NMDAR hyperfunction, whereas serine racemase knockouts (SR(-/-)) exhibit NMDAR hypofunction. We characterized the behavior of these lines in a Cocaine-induced (20 mg/kg) conditioned place preference (CPP) and locomotor sensitization paradigm. Compared with wild-type mice, GlyT1(+/-) mice displayed hastened extinction of CPP and robust Cocaine-induced reinstatement. SR(-/-) mice appeared to immediately "forget" the learned preference, because they did not exhibit Cocaine-induced reinstatement and also displayed attenuated locomotor sensitization. Treatment of GlyT1(+/-) mice with gavestinel (10 mg/kg on day 1; 5 mg/kg on days 2-17), a GMS antagonist, attenuated Cocaine-induced CPP and caused them to immediately "forget" the learned preference. Treatment of SR(-/-) mice with d-serine (300 mg/kg on day 1; 150 mg/kg on days 2-17) to normalize brain levels caused them to avoid the Cocaine-paired side of the chamber during extinction.
CONCLUSIONS:
These results highlight NMDAR dysfunction as a possible neural mechanism underlying comorbid schizophrenia and substance abuse. Also, these findings suggest drugs that directly or indirectly activate the NMDAR GMS could be an effective treatment of Cocaine abuse.

Product Name	Cocaine
Price:
CAS No.:	50-36-2
Catalog No.:	CFN00183
Molecular Formula:	C₁₇H₂₁NO₄
Molecular Weight:	303.35 g/mol
Purity:	>=98%
Type of Compound:	Alkaloids
Physical Desc.:	Powder
Source:	The leaves of the coca plant.
Solvent:	Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
Download:
Similar structural:	Comparison (Web) (SDF)
Guestbook:

Size /Price /Stock	10 mM * 100 uL in DMSO / Inquiry / In-stock 10 mM * 1 mL in DMSO / Inquiry / In-stock
Related Libraries	Local anaesthetics Compound Library Vasocontraction Compound Library Alkaloids Compound Library NMDAR Inhibitor Library HIV Inhibitor Library gp120/CD4 Inhibitor Library

	1 mg	5 mg	10 mg	20 mg	25 mg
1 mM	3.2965 mL	16.4826 mL	32.9652 mL	65.9304 mL	82.4131 mL
5 mM	0.6593 mL	3.2965 mL	6.593 mL	13.1861 mL	16.4826 mL
10 mM	0.3297 mL	1.6483 mL	3.2965 mL	6.593 mL	8.2413 mL
50 mM	0.0659 mL	0.3297 mL	0.6593 mL	1.3186 mL	1.6483 mL
100 mM	0.033 mL	0.1648 mL	0.3297 mL	0.6593 mL	0.8241 mL

CFN00148	Anisodine	52646-92-1	319.36	C₁₇H₂₁NO₅
CFN00149	Apoatropine	500-55-0	271.36	C₁₇H₂₁NO₂
CFN00150	Apohyoscine	535-26-2	285.34	C₁₇H₁₉NO₃
CFN00151	Aponorhyoscine	25650-56-0	271.31	C₁₆H₁₇NO₃
CFN00171	Nortropacocaine	18470-33-2	231.29	C₁₄H₁₇NO₂
CFN00177	Bellendine	32152-73-1	205.26	C₁₂H₁₅NO₂
CFN00181	Brugine	14912-30-2	273.42	C₁₂H₁₉NO₂S₂
CFN00182	Chalcostrobamine	75638-72-1	269.34	C₁₇H₁₉NO₂
CFN00183	Cocaine	50-36-2	303.35	C₁₇H₂₁NO₄
CFN00184	Pseudococaine	478-73-9	303.35	C₁₇H₂₁NO₄