DOCSLIB.ORG

Pharmacology and Toxicology

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Pharmacology and Toxicology Biogenuix Medsystems Pvt. Ltd. PHARMACOLOGY & TOXICOLOGY Receptors & Transporters Enzyme Modulators • 7-TM Receptors • ATPase & GTPase • Adrenoceptors • Caspase • AMPK / Insulin Receptor • Cyclases • Cannabinoid • Kinases • Dopamine • Phosphatases • Enzyme Linked Receptors • Proteases • GABA • Nuclear Receptors Biochemicals Toxicology • Opioids & Drug • Cardiotoxicity • Serotonin Discovery Peptides • Hematopoietic • Transporters Kits • Hepatotoxicity • Myotoxicity library Toxins • Nephrotoxicity • Venoms Lead Screening Cell Biology • Natural Products • Angiogenesis • Antimicrobials Compound Ion Channels • Apoptosis Libraries • Calcium Channels • Cancer Chemoprevention • CFTR • Cell Cycle • Ionophores • Cell Metabolism • Ligand Gated Ion Channels • Cytoskeleton & Motor Proteins • NMDA Receptors • ECM & Cell Adhesion • Potassium Channels • Epigenetics • Sodium Channels • NSAIDs • TRP Channels • Signal Transduction • Signalling Pathways • Stem Cells ® BIOCHEMICALS & PEPTIDES Ac-D-E Adenosine 5'-diphosphate . disodium salt Aceclofenac Adenosine 5'-diphosphate . potassium salt A Acemetacin Adenosine 5'-monophosphate . disodium salt Acepromazine maleate Adenosine 5'-O-(3-thiotriphosphate) . tetralithium Acetanilide salt Acetaminophen Adenosine 5'-O-thiomonophosphate . dilithium salt Adenosine 5'-triphosphate . disodium salt A-23187, 4 Bromo Acetomycin D,L-1'-Acetoxychavicol Acetate Adenosine-3’,5’-cyclic Monophosphothioate, Rp- A-23187, Ca-Mg Isomer . sodium salt 15-Acetoxyscirpenol A-3 HCL Adenosine-5'-O-(3-thiotriphosphate) . tetralithium A-3 Hydrochloride Acetyl, a-Endorphin salt A-317491 sodium salt hydrate Acetylcholine chloride Adiphenine Hcl A419259 Acetylcysteine Adipokinetic Hormone A419259 13-Acetyl-9-dihydrobaccatin-III Adipokinetic Hormone II from Locusta migratoria a5IA 3-Acetyldeoxynivalenol Adipokinetic Hormone II from Schistocera gregaria A-582941 Acetyl-L-Carnitine Adipokinetic Hormone, AKH, locust A-582941 Acetyl-L-Carnitine Hydrochloride AdipoRon A-674563 3-O-Acetyl-11-keto-β-boswellic acid ADL5859 Hcl A-740003 3-O-Acetyl-β-boswellic acid Adoprazine A-769662 Acetylsalicylic Acid / Aspirin ADP-HPD . ammonium salt . dihydrate A 77-01 2'-Acetyltaxol DL-Adrenaline A-77 1726 Ac-GPK(Ac)-pNA Adrenalone Hcl A-779 Ac-GPK-pNA Adrenic acid (22:4, n-6) A-803467 Aciclovir Adrenomedullin (13-52), human A-803467 Ac-IEAR-pNA Adrenomedullin (1-52), human A-83-01 Ac-IETD-pNA Adrenomedullin (22-52), human A-841720 Acipimox Adrenorphin A-867744 Acitazanolast Adriamycin A-922500 Acitretin ADWX-1 A-966492 Acivicin ADX-47273 A-967079 Aclacinomycin A AEBSF Hydrochloride AA-861 Ac-LEHD-PNA AEE788 AACOCF3 Acolbifene (EM 652, SCH57068) Aerophobin-2 AAF-CMK Aconitine Aeroplysinin 17-AAG ACP Aeroplysinin-1 AAL-993 (1S,3R)-ACPD Aerothionin a-ANF(1-28), human Ac-S-D-K-P Aeruginosamide B a-Apo-oxytetracycline ACT-335827 Aeruginosamide C Aaptamine ACTB-1003 Aeruginosamide D Ab05831 ACTH (1-10), human Aeruginosamide E Abacavir ACTH (1-13), human Aeruginosin 722 Abacavir sulfate ACTH (1-14) Aesculin Abamectin ACTH (1-16), human AEZS-108 Abarelix Acetate ACTH (1-17), human 4AF DA ABC294640 ACTH (1-24), human AF-DX 384 AB-FUBINACA ACTH (1-39), rat AFC (7-Amino-4-trifluoromethyl coumarin) Standard ABH . ammonium salt ACTH (1-4) Aflatoxin B1 Abiraterone ACTH (18-39), human Aflatoxin B2 Abiraterone Acetate ACTH (4-10), human Aflatoxin G1 Abscisic acid ACTH(1-39), human Aflatoxin G2 ABT Actinomycin D Aflatoxin M1 ABT-199 Actinonin Aflatoxin M2 ABT-263 Ac-VEID-pNA Afegostat ABT333 ACY-1215 Afzelin ABT-418 Hcl Acycloguanosine/Acyclovir AG-014699 ABT-492 Ac-YVAD-pNA AG-1024 (Tyrphostin) ABT-737 Adapalene AG-126 ABT-751 Adaphostin AG-1288 ABT-888 Adarotene AG-1296 Ac220 Adefovir Ag14361 AC-42 Adefovir dipivoxil AG-1478 AC-55469 Adenine AG-17 ACA Adenine sulfate AG-370 Acadesine Adenosine AG-490 Acarbose Adenosine 3',5'-cyclic Monophosphate . sodium salt Phone : +91-11-4875-4875 Email : [email protected] Fax : +91-11-2561-2008 AG-494 Altersolanol A Aminocaproic acid AG-825 Altrenogest 2-Aminoethoxydiphenyl borate AG-879 Altretamine DL-Aminoglutethimide AG 957 Aluminium chloride . hexahydrate Aminoguanidine . bicarbonate AGI-6780 Alvelestat Aminoguanidine . hemisulfate A-G-D-V Alvimopan Aminoguanidine . hydrochloride O-agatoxin IVA (O-aga IVA or omega agatoxin IVA) Alyssin 5-Aminolevulinic acid hydrochloride Agelasine D Alyssin sulfone 4'-Amino-6-hydroxyflavone Agelongine Alytesin 4-Amino-1,8-naphthalimide Agitoxin-2 Am095 6-Aminonicotinamide AGI-5198 (IDH-C35) AM 1220 4-Aminophenylphosphate . sodium salt AGK2 AM-1241 Aminophylline AG-L-59687 AM 2201 Aminophylline Dihydrate Agnuside AM 2233 S-(3-Aminopropyl)-ITU . Dihydrobromide Agomelatine AM-251 Aminopterin AH-6809 AM-281 2-Aminopurine AHU-377 AM-404 Aminopurvalanol A AICAR AM-580 4-Aminopyridine AIDA AM-580 4-Aminosalicylic Acid 5-AIQ . hydrochloride AM-630 4-Aminosalicylic acid sodium dihydrate AK-1 AM 694 5-Aminosalicylic acid AK-7 Am966 4-Amino-TEMPO, free radical A-K-R-R-R-L-S-S-L-R-A Alpha Mannosyl Ceramide Amiodarone Hydrochloride Akt-l-1 β-Amanitin Amisulpride AKT inhibitor VIII Amantadine Hydrochloride Amitraz A-L-A-L Amantadine Sulfate Amitriptyline Hydrochloride Alamethicin Amastatin Hydrochloride Amlexanox L-Alaninol Ambrisentan Amlodipine Albendazole Ambroxol Hydrochloride Amlodipine besylate Alendronate Monosodium Trihydrate AMC (7-Amino-4-methylcoumarin) Standard Ammonium Glycyrrhizinate Alendronate sodium hydrate AMD 070 AmmTx3 Alfacalcidol AMD 3465 Hexahydrobromide Amonafide Alfuzosin Hcl AMD3100 (Plerixafor) Amorolfine Hydrochloride Alibendol Alpha Melanocyte stimulating hormone Amoxapine (+)-Alliin Alpha Methylbenzyl isothiocyanate Amoxicillin Aliskiren Amentoflavone AMPA Aliskiren hemifumarate Ametantrone 5'-AMP Standard Alizarin Amfebutamone Ampalex (CX-516) ALK5 Inhibitor I AMG-073 (Cinacalcet) Amphotericin B ALK5 Inhibitor II AMG-073 Hcl Ampicillin . sodium salt Allatostatin I AMG-208 Ampicillin Trihydrate Allethrin AMG-208 Ampiroxicam Allicin AMG232 Amprenavir L-Alliin AMG-458 Amprolium Hcl L(+)Alliin /3-(2-Propenylsulfinyl) alanine AMG-47a Amrinone Almorexant AMG517 Amrubicin Almorexant Hcl AMG-8718 Amsacrine Allopurinol AMG-900 Amsilarotene (TAC-101) Allopurinol sodium AMG-9810 AMT . hydrochloride Alloxan Monohydrate AMG-Tie2-1 Amthamine all-trans-Retinol / Vitamin A AMI-1 Amygdalin Allyl disulfide AMI-193 Amylin (8-37), human 3-(4-Allylpiperazin-1-yl)-2-quinoxalinecarbonitrile Amidepsine A Amylin (8-37), rat Almotriptan malate (Axert) Amidepsine D Amylin (IAPP)(Feline) Aloe-emodin Amidopyrine Amylin, human Aloeresin A Amifostine Amylin, rat Aloesin Amikacin Disulfate b-Amyloid (1-40), rat Alogliptin Amyloid b-Peptide (1-42) (human) b-Amyloid (1-40), Ultra Pure, TFA Alogliptin Benzoate Amiloride HCl Dihydrate b-Amyloid (1-42), human Aloin (Barbaloin) Amiloride hydrochloride dihydrate β-Amyloid (25-35) Aloisine Amiloride, 5-(N,N-Dimethyl) hydrochloride β-Amyloid Peptide (1-42), rat Aloisine A Amiloride, 5-(N-Ethyl-N-isopropyl)- Amyloid-beta Protein (1-40) Alosetron Amiloride, 5-(N-Methyl-N-isobutyl)- a-Amyloid Precursor Protein Modulator a Amanitin 3-Amino-1H-pyrazolo[3,4-b]quinoxaline An2728 17-a-Ethynylestradiol 7-Aminoactinomycin D Anabaenopeptin 856 17 a-propionate 1-Aminobenzotriazole Anabaenopeptin 872 Alrestatin 3-Aminobenzamide Anabaenopeptin A Alsterpaullone 7-Aminocephalosporanic acid Anabaenopeptin B Altenusin 1-Aminocyclopentanecarboxylic acid Anabaenopeptin F Alternariol (2S)-(+)-Amino-5-iodoacetamidopentanoic acid Anabasine hydrochloride Alternariol monomethyl ether (2S)-(+)-Amino-6-iodoacetamidohexanoic acid Anacardic acid Alternariol-9-methyl ether 6-Aminocaproic acid Anacetrapib Phone : +91-11-4875-4875 Email : [email protected] Fax : +91-11-2561-2008 Anagliptin Aphidicolin AS-605240 Anagrelide Apicidin AS-703026 Anamorelin Apigenin As703026 Anamorelin Hcl Apiin Alpha Santonin Anandamide Apilimod Asaraldehyde Anandamide (18:2, n-6) Apixaban ASC-J9 Anandamide (22:4, n-6) Apocynin (Acetovanillone) Ascochin Anastrozole Apoptolidin Ascochlorin Anatoxin Apoptosis Ascomycin Andarine (GTx-007) Apoptosis Activator 2 L(+)-Ascorbic acid Andrastin A Apoptosis inducer set Ascorbyl palmitate Andrographolide APR-246 Asenapine maleate Andrographolide, Dehydro Apramycin Sulfate Asialo-GM1 Andrographolide-deoxy Apramycin Sulfate Asialo-GM2 Anethole-trithione Apremilast Asiatic acid Angelicin Aprepitant Asiaticoside Angiogenin Aprotinin ASP3026 Angiostatin APY29 ASP9521 Angiotensin Converting Enzyme Inhibitor Ar231453 Asparaginase Angiotensin I [Des-Asp1-], human AR-42 Aspartame Angiotensin I, human Ar7 Aspergillimide Angiotensin II (1-4), human AR-A014418 Asperlactone Angiotensin II (3-8), human AR-C117977 Asperosaponin VI Angiotensin II (4-8), human Arachidonamide Aspinonene Angiotensin II [Sar1 Ile8] Arachidonic acid (20:4, n-6) Aspirin Angiotensin II [Sar1] Arachidonoyl-AMC Aspterric Acid Angiotensin II, human Arachidonyl-2-chloroethylamide AST-1306 Angiotensin II, human [Val5] Arachidonylcyclopropylamide AST-6 [Ile7] Angiotensin III Aranciamycin Astemizole Angiotensin III, human Arbidol Asterric acid Angiotensin, Canine, rat Arbidol Hcl Astibin Angiotensinogen (1-14), human Arbutin Astragaloside A Angoroside C AR-C155858 Astragaloside II Anguinomycin A 2-Arachidonoylglycerol Astragaloside III Anguizole Arctigenin Astragaloside IV Anidulafungin Arctiin Asunaprevir Aniracetam Arcyriaflavin A At101 Aniracetama Arecoline At13148 Anisodamine Arenobufagin AT-13387 Anisomycin Arformoterol Tartrate AT-406 Anorexigenic Peptide Argatroban AT 56 ANP (1-11), rat Aripiprazole
Load more

Recommended publications
  • WADA Technical Letter – TL07 ANDARINE
    WADA Technical Letter – TL07 Document Number: TL07 Version Number: 3.0 Written by: WADA Science Approved by: WADA Executive Committee Reviewed by: WADA Laboratory Expert Group Date: 21 December 2020 Effective Date: 1 January 2021 ANDARINE - FLUTAMIDE 1.0 Introduction WADA wishes to draw the attention of the Laboratories to the following observations and instructions on the analysis and reporting of SARM S4 (Andarine) Metabolites O-dephenylandarine and O- dephenylandarine glucuronide. The andarine Metabolites O-dephenylandarine and of O-dephenylandarine glucuronide may also be present in a Sample as a Metabolite of the anti-androgen Flutamide (Drogenil®, Eulexin®, Euflex®, Flutamin®, Flugere®), used primarily in the treatment of prostate cancer [1]. Since flutamide is not a Prohibited Substance in sports, the Laboratories shall not report an Adverse Analytical Finding (AAF) for andarine based on the monitoring of O-dephenylandarine [2]. Figure 1. Proposed metabolic pathway of flutamide and andarine (adapted from Perrenoud et al. [1]). 2.0 Analysis and Reporting Requirements Report the result as an AAF for andarine only when the presence of andarine (parent compound), and/or its glucuronic acid conjugate, and/or its deacetylated and/or hydroxylated Metabolites, and/or its bishydroxylated product [2] are confirmed in the Sample (regardless of the presence of flutamide and/or its Metabolite 2-hydroxyflutamide); [Comment: Laboratories shall not report an AAF for andarine based only on the presence of O- dephenylandarine.] 3.0 References [1] Perrenoud L. et al. Risk of false positive results to SARM S4 in case of therapeutic use of antineoplastic/antiandrogen drug containing flutamide: a case study.
    [Show full text]
  • 615 Neuroscience-Cayman-Bertin
    Thomas G. Brock, Ph.D. Introduction to Neuroscience In our first Biology classes, we learned that lipids form the membranes around cells. For many students, interests quickly moved to the intracellular constituents ‘that really matter’, or to how cells or systems work in health and disease. If there was further thought about lipids, it might have been limited to more personal issues, like an expanding waistline. It was easy to forget about lipids in the complexities of, say, Alzheimer’s Disease, where tau protein is hyperphosphorylated by a host of kinases before forming neurofibrillary tangles and amyloid precursor protein is processed by assorted secretases, ultimately aggregating to form neurodegenerating plaques. What possible role could lipids have in all this? After all, lipids just form the membranes around cells. Fortunately, neuroscientists study complex systems. Whether working at the molecular, cellular, or organismal level, the research focus always returns to the intricately interconnected bigger picture. Perhaps surprisingly, lipids keep emerging as part of the bigger picture. At least, the smaller lipids do. Many of the smaller lipids, including the cannabinoids and eicosanoids, act as paracrine hormones, modulating cell functions in a receptor-mediated fashion. In this sense, they are rather like the peptide hormones in their diversity and actions. In the neurosystem, this means that these signaling lipids determine if synapses fire or not, when cells differentiate or die, and whether tissues remain healthy or become inflamed. Returning to the question posed above about lipids in Alzheimer’s, these mediators have roles at many levels in the course of the disease, as presented in an article on page 42 of this catalog.
    [Show full text]
  • INVESTIGATION of NATURAL PRODUCT SCAFFOLDS for the DEVELOPMENT of OPIOID RECEPTOR LIGANDS by Katherine M
    INVESTIGATION OF NATURAL PRODUCT SCAFFOLDS FOR THE DEVELOPMENT OF OPIOID RECEPTOR LIGANDS By Katherine M. Prevatt-Smith Submitted to the graduate degree program in Medicinal Chemistry and the Graduate Faculty of the University of Kansas in partial fulfillment of the requirements for the degree of Doctor of Philosophy. _________________________________ Chairperson: Dr. Thomas E. Prisinzano _________________________________ Dr. Brian S. J. Blagg _________________________________ Dr. Michael F. Rafferty _________________________________ Dr. Paul R. Hanson _________________________________ Dr. Susan M. Lunte Date Defended: July 18, 2012 The Dissertation Committee for Katherine M. Prevatt-Smith certifies that this is the approved version of the following dissertation: INVESTIGATION OF NATURAL PRODUCT SCAFFOLDS FOR THE DEVELOPMENT OF OPIOID RECEPTOR LIGANDS _________________________________ Chairperson: Dr. Thomas E. Prisinzano Date approved: July 18, 2012 ii ABSTRACT Kappa opioid (KOP) receptors have been suggested as an alternative target to the mu opioid (MOP) receptor for the treatment of pain because KOP activation is associated with fewer negative side-effects (respiratory depression, constipation, tolerance, and dependence). The KOP receptor has also been implicated in several abuse-related effects in the central nervous system (CNS). KOP ligands have been investigated as pharmacotherapies for drug abuse; KOP agonists have been shown to modulate dopamine concentrations in the CNS as well as attenuate the self-administration of cocaine in a variety of species, and KOP antagonists have potential in the treatment of relapse. One drawback of current opioid ligand investigation is that many compounds are based on the morphine scaffold and thus have similar properties, both positive and negative, to the parent molecule. Thus there is increasing need to discover new chemical scaffolds with opioid receptor activity.
    [Show full text]
  • Opportunities and Pharmacotherapeutic Perspectives
    biomolecules Review Anticoronavirus and Immunomodulatory Phenolic Compounds: Opportunities and Pharmacotherapeutic Perspectives Naiara Naiana Dejani 1 , Hatem A. Elshabrawy 2 , Carlos da Silva Maia Bezerra Filho 3,4 and Damião Pergentino de Sousa 3,4,* 1 Department of Physiology and Pathology, Federal University of Paraíba, João Pessoa 58051-900, Brazil; [email protected] 2 Department of Molecular and Cellular Biology, College of Osteopathic Medicine, Sam Houston State University, Conroe, TX 77304, USA; [email protected] 3 Department of Pharmaceutical Sciences, Federal University of Paraíba, João Pessoa 58051-900, Brazil; [email protected] 4 Postgraduate Program in Bioactive Natural and Synthetic Products, Federal University of Paraíba, João Pessoa 58051-900, Brazil * Correspondence: [email protected]; Tel.: +55-83-3216-7347 Abstract: In 2019, COVID-19 emerged as a severe respiratory disease that is caused by the novel coronavirus, Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2). The disease has been associated with high mortality rate, especially in patients with comorbidities such as diabetes, cardiovascular and kidney diseases. This could be attributed to dysregulated immune responses and severe systemic inflammation in COVID-19 patients. The use of effective antiviral drugs against SARS-CoV-2 and modulation of the immune responses could be a potential therapeutic strategy for Citation: Dejani, N.N.; Elshabrawy, COVID-19. Studies have shown that natural phenolic compounds have several pharmacological H.A.; Bezerra Filho, C.d.S.M.; properties, including anticoronavirus and immunomodulatory activities. Therefore, this review de Sousa, D.P. Anticoronavirus and discusses the dual action of these natural products from the perspective of applicability at COVID-19.
    [Show full text]
  • Ilamycin C Induces Apoptosis and Inhibits Migration and Invasion In
    Xie et al. Journal of Hematology & Oncology (2019) 12:60 https://doi.org/10.1186/s13045-019-0744-3 RESEARCH Open Access Ilamycin C induces apoptosis and inhibits migration and invasion in triple-negative breast cancer by suppressing IL-6/STAT3 pathway Qing Xie1†, Zhijie Yang2†, Xuanmei Huang1, Zikang Zhang1, Jiangbin Li1, Jianhua Ju2*, Hua Zhang1* and Junying Ma2* Abstract Background: Triple-negative breast cancer (TNBC) is the most aggressive subtype of breast cancer with poor prognosis, and its treatment remains a challenge due to few targeted medicines and high risk of relapse, metastasis, and drug resistance. Thus, more effective drugs and new regimens for the therapy of TNBC are urgently needed. Ilamycins are a kind of cyclic peptides and produced by Streptomyces atratus and Streptomyces islandicus with effective anti-tuberculosis activity. Ilamycin C is a novel compound isolated from the deep South China Sea- derived Streptomyces atratus SCSIO ZH16 and exhibited a strong cytotoxic activity against several cancers including breast cancer cell line MCF7. However, the cytotoxic activity of Ilamycin C to TNBC cells and a detailed antitumor mechanism have not been reported. Methods: CCK-8 assays were used to examine cell viability and cytotoxic activity of Ilamycin C to TNBC, non-TNBC MCF7, and nonmalignant MCF10A cells. EdU assays and flow cytometry were performed to assess cell proliferation and cell apoptosis. Transwell migration and Matrigel invasion assays were utilized to assess the migratory and invading capacity of TNBC cells following the treatment of Ilamycin C. The expressions of proteins were detected by western blot. Results: In this study, we found that Ilamycin C has more preferential cytotoxicity in TNBC cells than non-TNBC MCF7 and nonmalignant MCF10A cells.
    [Show full text]
  • Cannabinoids and Endocannabinoid System Changes in Intestinal Inflammation and Colorectal Cancer
    cancers Review Cannabinoids and Endocannabinoid System Changes in Intestinal Inflammation and Colorectal Cancer Viktoriia Cherkasova, Olga Kovalchuk * and Igor Kovalchuk * Department of Biological Sciences, University of Lethbridge, Lethbridge, AB T1K 7X8, Canada; [email protected] * Correspondence: [email protected] (O.K.); [email protected] (I.K.) Simple Summary: In recent years, multiple preclinical studies have shown that changes in endo- cannabinoid system signaling may have various effects on intestinal inflammation and colorectal cancer. However, not all tumors can respond to cannabinoid therapy in the same manner. Given that colorectal cancer is a heterogeneous disease with different genomic landscapes, experiments with cannabinoids should involve different molecular subtypes, emerging mutations, and various stages of the disease. We hope that this review can help researchers form a comprehensive understanding of cannabinoid interactions in colorectal cancer and intestinal bowel diseases. We believe that selecting a particular experimental model based on the disease’s genetic landscape is a crucial step in the drug discovery, which eventually may tremendously benefit patient’s treatment outcomes and bring us one step closer to individualized medicine. Abstract: Despite the multiple preventive measures and treatment options, colorectal cancer holds a significant place in the world’s disease and mortality rates. The development of novel therapy is in Citation: Cherkasova, V.; Kovalchuk, critical need, and based on recent experimental data, cannabinoids could become excellent candidates. O.; Kovalchuk, I. Cannabinoids and This review covered known experimental studies regarding the effects of cannabinoids on intestinal Endocannabinoid System Changes in inflammation and colorectal cancer. In our opinion, because colorectal cancer is a heterogeneous Intestinal Inflammation and disease with different genomic landscapes, the choice of cannabinoids for tumor prevention and Colorectal Cancer.
    [Show full text]
  • Specifications of Approved Drug Compound Library
    Annexure-I : Specifications of Approved drug compound library The compounds should be structurally diverse, medicinally active, and cell permeable Compounds should have rich documentation with structure, Target, Activity and IC50 should be known Compounds which are supplied should have been validated by NMR and HPLC to ensure high purity Each compound should be supplied as 10mM solution in DMSO and at least 100µl of each compound should be supplied. Compounds should be supplied in screw capped vial arranged as 96 well plate format.
    [Show full text]
  • Thromboxane A2 Receptor Antagonist SQ29548 Attenuates SH‑SY5Y Neuroblastoma Cell Impairments Induced by Oxidative Stress
    INTERNATIONAL JOURNAL OF MOleCular meDICine 42: 479-488, 2018 Thromboxane A2 receptor antagonist SQ29548 attenuates SH‑SY5Y neuroblastoma cell impairments induced by oxidative stress GAOYU CAI1*, AIJUAN YAN2*, NINGZHEN FU3 and YI FU1 1Department of Neurology, Rui Jin Hospital, Shanghai Jiao Tong University, Shanghai 200025; 2Department of Neurology, Xin Hua Hospital, Shanghai Jiao Tong University, Shanghai 200082; 3Department of Pancreatic Surgery, Rui Jin College of Clinical Medicine, Rui Jin Hospital, Shanghai Jiao Tong University, Shanghai 200025, P.R. China Received September 28, 2017; Accepted March 21, 2018 DOI: 10.3892/ijmm.2018.3589 Abstract. Thromboxane A2 receptor (TXA2R) serves a vital SQ29548, an antagonist of TXA2R, improved the antioxidant role in numerous neurological disorders. Our previous study capacities of SH-SY5Y cells and reduced the cell apoptosis indicated that SQ29548, an antagonist of TXA2R, attenuated through the inhibition of MAPK pathways. the induced neuron damage in cerebral infarction animals; however, the underlying mechanism remains unknown. Introduction Certain studies revealed a new role of TXA2R in the regula- tion of oxidative stress, which is one of the basic pathological Thromboxane A2 receptor (TXA2R), a member of the G processes in neurological disorders. Thus, the present study protein-coupled receptor family (1), is broadly distributed attempted to examine whether the inhibition of TXA2R with in platelets (2), as well as epithelial (3), smooth muscle (4), SQ29548 helped to protect the nerve cells against oxidative glial and nerve cells in the brain (5). TXA2R is regarded as a stress. SQ29548 was utilized as a TXA2R antagonist, and traditional coagulation and inflammation‑associated receptor, relevant assays were performed to detect the cell viability, which is also closely associated with neurological disorders.
    [Show full text]
  • The Detection and Determination of Esters
    Louisiana State University LSU Digital Commons LSU Historical Dissertations and Theses Graduate School 1958 The etD ection and Determination of Esters. Mohd. Mohsin Qureshi Louisiana State University and Agricultural & Mechanical College Follow this and additional works at: https://digitalcommons.lsu.edu/gradschool_disstheses Recommended Citation Qureshi, Mohd. Mohsin, "The eD tection and Determination of Esters." (1958). LSU Historical Dissertations and Theses. 501. https://digitalcommons.lsu.edu/gradschool_disstheses/501 This Dissertation is brought to you for free and open access by the Graduate School at LSU Digital Commons. It has been accepted for inclusion in LSU Historical Dissertations and Theses by an authorized administrator of LSU Digital Commons. For more information, please contact [email protected]. Copright by Mohcl Mohsin Qureshi 1959 THE DETECTION AND DETERMINATION OF ESTERS A Dissertation Submitted to the Graduate Faculty of the Louisiana State University and Agricultural and Mechanical College in partial fulfillment of the requirements for the degree of Doctor of Philosophy in The Department of Chemistry by Mohd. Mohsin Qureshi M.Sc., Aligarh University, 1944 August, 1958 ACKNOWLEDGMENT The author wishes to express his sincere apprecia­ tion and gratitude to Dr. Philip W. West under whose guidance this research was carried out. He is grateful to Dr. James G. Traynham for sup­ plying him with a number of esters and for his many helpful suggestions. The financial support given to him by the Continental Oil Company is gratefully acknowledged. He offers his sincere thanks to Miss Magdalena Usategul for her valuable suggestions and her ungrudging help during the course of this investigation. Dr. Anil K.
    [Show full text]
  • Analytical Performance of an Immunoassay to Measure Proenkephalin ⁎ Leslie J
    Clinical Biochemistry xxx (xxxx) xxx–xxx Contents lists available at ScienceDirect Clinical Biochemistry journal homepage: www.elsevier.com/locate/clinbiochem Analytical performance of an immunoassay to measure proenkephalin ⁎ Leslie J. Donatoa, ,Jeffrey W. Meeusena, John C. Lieskea, Deborah Bergmannc, Andrea Sparwaßerc, Allan S. Jaffea,b a Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN 55905, United States b Division of Cardiology, Mayo Clinic, Rochester, MN 55905, United States c Sphingotec GmbH, Hennigsdorf, Germany ARTICLE INFO ABSTRACT Keywords: Background: Endogenous opioids, enkephalins, are known to increase with acute kidney injury. Since the mature Biomarkers pentapeptides are unstable, we evaluated the performance of an assay that measures proenkephalin 119–159 Proenkephalin (PENK), a stable peptide formed concomitantly with mature enkephalins. Enkephalin Methods: PENK assay performance was evaluated on two microtiterplate/chemiluminescence sandwich im- Pro-enkephalin munoassay formats that required 18 or 1 h incubation times. PENK concentration was measured in plasma from penKid healthy individuals to establish a reference interval and in patients with varied levels of kidney function and Assay validation comorbidities to assess the association with measured glomerular filtration rate (mGFR) using iothalamate clearance. Results: Assay performance characteristics in plasma were similar between the assay formats. Limit of quanti- tation was 26.0 pmol/L (CV = 20%) for the 1 h assay and 17.3 pmol/L (CV = 3%) for the 18 h assay. Measurable ranges were 26–1540 pmol/L (1 h assay) and 18–2300 pmol/L (18 h assay). PENK concentrations are stable in plasma stored ambient to 10 days, refrigerated to at least 15 days, and frozen to at least 90 days.
    [Show full text]
  • Molecular Dynamics Simulations in Drug Discovery and Pharmaceutical Development
    processes Review Molecular Dynamics Simulations in Drug Discovery and Pharmaceutical Development Outi M. H. Salo-Ahen 1,2,* , Ida Alanko 1,2, Rajendra Bhadane 1,2 , Alexandre M. J. J. Bonvin 3,* , Rodrigo Vargas Honorato 3, Shakhawath Hossain 4 , André H. Juffer 5 , Aleksei Kabedev 4, Maija Lahtela-Kakkonen 6, Anders Støttrup Larsen 7, Eveline Lescrinier 8 , Parthiban Marimuthu 1,2 , Muhammad Usman Mirza 8 , Ghulam Mustafa 9, Ariane Nunes-Alves 10,11,* , Tatu Pantsar 6,12, Atefeh Saadabadi 1,2 , Kalaimathy Singaravelu 13 and Michiel Vanmeert 8 1 Pharmaceutical Sciences Laboratory (Pharmacy), Åbo Akademi University, Tykistökatu 6 A, Biocity, FI-20520 Turku, Finland; ida.alanko@abo.fi (I.A.); rajendra.bhadane@abo.fi (R.B.); parthiban.marimuthu@abo.fi (P.M.); atefeh.saadabadi@abo.fi (A.S.) 2 Structural Bioinformatics Laboratory (Biochemistry), Åbo Akademi University, Tykistökatu 6 A, Biocity, FI-20520 Turku, Finland 3 Faculty of Science-Chemistry, Bijvoet Center for Biomolecular Research, Utrecht University, 3584 CH Utrecht, The Netherlands; [email protected] 4 Swedish Drug Delivery Forum (SDDF), Department of Pharmacy, Uppsala Biomedical Center, Uppsala University, 751 23 Uppsala, Sweden; [email protected] (S.H.); [email protected] (A.K.) 5 Biocenter Oulu & Faculty of Biochemistry and Molecular Medicine, University of Oulu, Aapistie 7 A, FI-90014 Oulu, Finland; andre.juffer@oulu.fi 6 School of Pharmacy, University of Eastern Finland, FI-70210 Kuopio, Finland; maija.lahtela-kakkonen@uef.fi (M.L.-K.); tatu.pantsar@uef.fi
    [Show full text]
  • 204569Orig1s000
    CENTER FOR DRUG EVALUATION AND RESEARCH APPLICATION NUMBER: 204569Orig1s000 MEDICAL REVIEW(S) Cross Discipline Team Leader Review 3. CMC/Device Dr. Khairuzzaman found the drug product portion of the NDA to be acceptable, and without need for phase 4 commitments. Dr. Sapru’s review stated that with the exception of a pending issue concerning the control of potential genotoxic impurity (b) (4) the NDA was approvable in terms of drug substance. Dr. Suarez found that the NDA was acceptable from a biopharmaceutics perspective. The Office of Compliance issuance of an acceptable recommendation for drug substance manufacturing and testing facilities was pending at the time of this review. 4. Nonclinical Pharmacology/Toxicology Dr. Richard Siarey completed the primary nonclinical review, and Dr. Lois Freed completed a supervisory memo. Dr. Siarey’s overall conclusion was that from a nonclinical perspective, approval of the suvorexant NDA was recommended. However, he found evidence that catapelxy was observed in dogs exposed to MK-4305 (suvorexant) near Tmax, although he concluded that additional information could have been gained by studying the drug in an experimental model that has been used for diagnosing cataplexy in dogs. Dr. Siarey suggested that since cataplexy occurred in dogs near Tmax, a time at which if used for insomnia patients would ordinarily be in bed, safety concern for humans was reduced. Dr. Siarey also found that the neurobehavioral assessment in the pre- and post-natal developmental study was not complete, as the passive avoidance tests was performed too early in development, while learning/acquisition tests and retention/memory tests were not conducted.
    [Show full text]