Pseudoephedrine 60mg / Acrivastine 8mg capsules
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Benadryl Allergy Relief Plus Decongestant capsules
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View full Drug TariffSource: NHS Drug Tariff via NHSBSA. Derived from dm+d VMPP (Virtual Medicinal Product Pack) pricing data. Contains public sector information licensed under the Open Government Licence v3.0.
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Active and completed clinical studies from ClinicalTrials.gov
Source: ClinicalTrials.gov, a database of the U.S. National Library of Medicine (NLM), National Institutes of Health (NIH). Data accessed via ClinicalTrials.gov API v2. Trial information is provided for research purposes and does not constitute medical advice.
Academic studies and reviews for this medicine's active substance
Showing all 18 studies.
Reviews & meta-analyses: 2 · Randomised trials: 1 · 1989–2024
Showing all 18 studies, sorted by most relevant.
Takeshi Sakayori, Y. Ikeda, Ryosuke Arakawa, et al.
Scientific Reports, 2024
- Brain
- Central Nervous System Stimulants
- Doping in Sports
Intellectual drug doping in athletics by using stimulants that affect central nervous system functions has been diversified. Stimulants are regulated by the World Anti-Doping Agency according to their levels of urinary concentration. Positron emission tomography could evaluate how stimulants affect central nervous system functions. We aimed to evaluate the effect of stimulants on brain function by examining the difference in brain dopamine transporter occupancy by PET after administration of dl-methylephedrine or pseudoephedrine at the clinical maximum daily dose. Four PET scans without and with drug administration (placebo, dl-methylephedrine 150 mg and pseudoephedrine 240 mg) were performed. The concentrations of dl-methylephedrine and pseudoephedrine in plasma and urine were measured. DAT occupancies in the striatum with placebo, dl-methylephedrine and pseudoephedrine were calculated by PET images. The urinary concentration of dl-methylephedrine (12.7 µg/mL) exceeded the prohibited concentration (10 µg/mL), but the DAT occupancy with dl-methylephedrine (6.1%) did not differ (p = 0.92) from that with placebo (6.2%). By contrast, although the urinary concentration of pseudoephedrine (144.8 µg/mL) was below the prohibited concentration (150 μg/mL), DAT occupancy with pseudoephedrine was 18.4%, which was higher than that with placebo (p = 0.009). At the maximum clinical dose, dl-methylephedrine was shown to have weaker effects on brain function than pseudoephedrine.
Abstract licence: CC BY-NC-ND
K. Głowacka, A. Wiela-Hojeńska
International Journal of Molecular Sciences, 2021
- Bronchodilator Agents
- Methamphetamine
- Risk Assessment
Pseudoephedrine (PSE) is a drug with a long history of medical use; it is helpful in treating symptoms of the common cold and flu, sinusitis, asthma, and bronchitis. Due to its central nervous system (CNS) stimulant properties and structural similarity to amphetamine, it is also used for non-medical purposes. The substance is taken as an appetite reducer, an agent which eliminates drowsiness and fatigue, to improve concentration and as a doping agent. Due to its easier availability, it is sometimes used as a substitute for amphetamine or methamphetamine. Pseudoephedrine is also a substrate (precursor) used in the production of these drugs. Time will tell whether legal restrictions on the sale of this drug will reduce the scale of the problem associated with its misuse.
Abstract licence: CC BY
Shu-guang Yan, Wenbao Wang, Jing-tao Li, et al.
Chinese Medicine, 2021
BACKGROUND: Acute lung injury (ALI) is an acute multifactorial infectious disease induced by trauma, pneumonia, shock, and sepsis. This study aimed to investigate the protective effects of pseudoephedrine and emodin combined treatment in experimental ALI, as well as the mechanisms underlying the regulation of inflammation and pulmonary edema via the VIP/cAMP/PKA pathway. METHODS: The wistar rats were randomly divided into fifteen groups (n = 5). Rats in each group were given intragastric administration 1 h before LPS injection. Those in the control and LPS groups were given intragastric administrations of physiological saline, rats in other groups were given intragastrically administered of differential dose therapeutic agents. The rats in the LPS and treatment groups were then injected intraperitoneally with LPS (7.5 mg/kg) to induce ALI. After being treated with pseudoephedrine and emodin for 12 h, all animals were sacrifice. Anal temperatures were taken on an hourly basis for 8 h after LPS injection. Pathological examination of lung specimen was performed by H&E staining. Cytokines (IL-1β, TNF-α, IL-6, iNOS, IL-10, Arg-1, CD86, CD206, F4/80, VIP) in lung tissue were assayed by ELISA and immunofluorescence. The expression of VIP, CAMP, AQP-1, AQP-5, p-PKA, PKA, p-IκBα, IκBα, p-p65, p65, p-P38, P38, p-ERK1/2, ERK1/2, p-JNK1/2, JNK1/2 protein in lung was determined by western blotting. RESULTS: After rats being treated with pseudoephedrine + emodin, reduced of fever symptoms. The contents of inflammatory cytokines (IL-1β, TNF-α, IL-6, iNOS) were decreased and anti-inflammatory cytokines (IL-10, Arg-1) were significantly increased in serum. Pseudoephedrine + emodin treatment effectively promoted VIP cAMP and p-PKA protein expression in lung tissues, and significantly inhibited NF-κB, MAPK phosphorylation, Pseudoephedrine + emodin treatment can inhibit M1 polarization and promoted M2 polarization via the VIP/cAMP/PKA signaling pathway. CONCLUSIONS: The combination of Pseudoephedrine and emodin was effective in ameliorating LPS-induced ALI in rats by inducing VIP/cAMP/PKA signaling. Inhibiting the NF-κB, MAPK inflammatory pathway, relief of pulmonary edema suppressing macrophage M1 polarization, and promoting macrophage M2 polarization.
Abstract licence: CC BY
Ramesh Rijal, Manoj Sah, H. P. Lamichhane
Heliyon, 2023
The ground state molecular energy, vibrational frequencies and HOMO-LUMO analysis of the title compound have been calculated with density functional theory in the B3LYP/6-311 + G (d,p) basis set using Gaussian 09 W software. The FT-IR spectrum of pseudoephedrine has been computed in the gas phase and in the presence of solvent water both in neutral and anionic structures. The TED assignments of the vibrational spectra have been assigned in the selected intense region. On isotopic substitution of carbon atoms, the shifting of frequencies is distinctly observed. The reported values and HOMO-LUMO mappings reveal the possibility of different charge transfers occurring within the molecule. A MEP map is depicted and the Mulliken atomic charge is also calculated. The UV-Vis spectra have been illustrated and explained from the frontier molecular orbitals using a TD-DFT approach.
Abstract licence: CC BY-NC-ND
J. Neumann, Wilhelm Hußler, B. Hofmann, et al.
Journal of Cardiovascular Pharmacology, 2023
- Alkaloids
- Amphetamine
- Cocaine
Brendan M. Miller, James F. Carter, Sarah L. Cresswell, et al.
Forensic science international, 2024
Carl H. Fleischer, Sean T Holmes, Kirill Levin, et al.
Faraday discussions, 2024
Cl SSNMR data as experimental input. This proof-of-concept work suggests the possibility of employing QNMRX-CSP to solve the structures of organic HCl salts in dosage forms - something which is often beyond the capabilities of conventional, diffraction-based characterization methods.
Abstract licence: CC BY-NC
M. Nose, R. Kobayashi, Momoka Tada, et al.
Journal of Natural Medicines, 2023
- Drugs, Chinese Herbal
- Ephedrine
- Japan
C. Bojkowski, T. Gibbs, K. Hellstern, et al.
The Journal of international medical research, 1989
Sherif Ramzy, A. Abdelazim, Mohamed A. Hasan
BMC Chemistry, 2022
Fexofenadine hydrochloride and pseudoephedrine hydrochloride are prescribed in a combined dosage form for the treatment of allergic rhinitis. In the present work, a sensitive synchronous fluorescence spectroscopic method was applied in conjunction with first derivative for quantitative estimation of fexofenadine hydrochloride and pseudoephedrine hydrochloride in pure form, pharmaceutical tablets and spiked human plasma. Fexofenadine hydrochloride showed its conventional emission spectrum at 294 nm when excited at 267 nm. On the other hand, pseudoephedrine hydrochloride showed its conventional emission spectra at 286 nm when excited at 261 nm. The fluorescence intensities were greatly enhanced by the use of sodium dodecyl sulphate as a micellar surfactant. Application of the synchronous mode to measure the fluorescence spectra of the above drugs provided sharp narrowing bands, but the overlap was not completely resolved. Derivatization of the synchronous spectra to the first order completely resolved the overlap of the fluorescence spectra and allowed simultaneous quantitative determination of the drugs under study. Fexofenadine hydrochloride and pseudoephedrine hydrochloride could be determined from their first-order synchronous spectra at 286 and 294 nm, respectively, without interfering with each other. The method showed linearity with an excellent correlation coefficient in the concentration range of 100-1500 ng/mL for Fexofenadine hydrochloride and 50-1000 ng/mL for pseudoephedrine hydrochloride. The method was successfully applied for the simultaneous determination of the studied drugs in pharmaceutical formulation, with mean percent recoveries for Fexofenadine hydrochloride and pseudoephedrine hydrochloride of 99.49 ± 0.931 and 98.67 ± 0.634, respectively, and in spiked human plasma, with mean percent recoveries for Fexofenadine hydrochloride and pseudoephedrine hydrochloride of 95.21 ± 1.938 and 94.89 ± 1.763, respectively. Furthermore, the greenness of the described method was assessed using four different tools namely, the national environmental method index, the analytical eco-scale, the green analytical procedure index and the AGREE evaluation method. The proposed method seemed to be superior to the reported HPLC method with respect to the metrics of the greenness characters.
Abstract licence: CC BY
Sources: aggregated from Europe PMC (EMBL-EBI), OpenAlex, Crossref, PubMed and other open scholarly databases. Retracted articles are excluded. Study information is provided for research purposes and does not constitute medical advice.
Scientific data (pharmacology, interactions, ADME) is not yet available for this medicine. Clinical sections are sourced from the NHS dm+d database.