Amodiaquine: A 4-aminoquinoline compound with anti-inflammatory properties.Antimalarials: Agents used in the treatment of malaria. They are usually classified on the basis of their action against plasmodia at different stages in their life cycle in the human. (From AMA, Drug Evaluations Annual, 1992, p1585)Sulfadoxine: A long acting sulfonamide that is used, usually in combination with other drugs, for respiratory, urinary tract, and malarial infections.Artemisinins: A group of SESQUITERPENES and their analogs that contain a peroxide group (PEROXIDES) within an oxepin ring (OXEPINS).Pyrimethamine: One of the FOLIC ACID ANTAGONISTS that is used as an antimalarial or with a sulfonamide to treat toxoplasmosis.Chloroquine: The prototypical antimalarial agent with a mechanism that is not well understood. It has also been used to treat rheumatoid arthritis, systemic lupus erythematosus, and in the systemic therapy of amebic liver abscesses.Drug Combinations: Single preparations containing two or more active agents, for the purpose of their concurrent administration as a fixed dose mixture.Malaria, Falciparum: Malaria caused by PLASMODIUM FALCIPARUM. This is the severest form of malaria and is associated with the highest levels of parasites in the blood. This disease is characterized by irregularly recurring febrile paroxysms that in extreme cases occur with acute cerebral, renal, or gastrointestinal manifestations.Plasmodium falciparum: A species of protozoa that is the causal agent of falciparum malaria (MALARIA, FALCIPARUM). It is most prevalent in the tropics and subtropics.Fluorenes: A family of diphenylenemethane derivatives.Drug Resistance: Diminished or failed response of an organism, disease or tissue to the intended effectiveness of a chemical or drug. It should be differentiated from DRUG TOLERANCE which is the progressive diminution of the susceptibility of a human or animal to the effects of a drug, as a result of continued administration.SesquiterpenesParasitic Sensitivity Tests: Tests that demonstrate the relative effectiveness of chemotherapeutic agents against specific parasites.Senegal: A republic in western Africa, southwest of MAURITANIA and east of MALI. Its capital is Dakar.Drug Therapy, Combination: Therapy with two or more separate preparations given for a combined effect.Ethanolamines: AMINO ALCOHOLS containing the ETHANOLAMINE; (-NH2CH2CHOH) group and its derivatives.Cameroon: A republic in central Africa lying east of CHAD and the CENTRAL AFRICAN REPUBLIC and west of NIGERIA. The capital is Yaounde.Betazole: A histamine H2 agonist used clinically to test gastric secretory function.Histamine N-Methyltransferase: An enzyme that catalyzes the transfer of a methyl group from S-adenosylmethionine to histamine, forming N-methylhistamine, the major metabolite of histamine in man. EC 2.1.1.8.Parasitemia: The presence of parasites (especially malarial parasites) in the blood. (Dorland, 27th ed)Malaria: A protozoan disease caused in humans by four species of the PLASMODIUM genus: PLASMODIUM FALCIPARUM; PLASMODIUM VIVAX; PLASMODIUM OVALE; and PLASMODIUM MALARIAE; and transmitted by the bite of an infected female mosquito of the genus ANOPHELES. Malaria is endemic in parts of Asia, Africa, Central and South America, Oceania, and certain Caribbean islands. It is characterized by extreme exhaustion associated with paroxysms of high FEVER; SWEATING; shaking CHILLS; and ANEMIA. Malaria in ANIMALS is caused by other species of plasmodia.Ghana: A republic in western Africa, south of BURKINA FASO and west of TOGO. Its capital is Accra.Angola: A republic in southern Africa, southwest of DEMOCRATIC REPUBLIC OF THE CONGO and west of ZAMBIA. Its capital is Luanda.Gabon: A republic in west equatorial Africa, south of CAMEROON and west of the CONGO. Its capital is Libreville.Burkina Faso: A republic in western Africa, south and east of MALI and west of NIGER. Its capital is Ouagadougou. It was formerly called Upper Volta until 1984.Protozoan Proteins: Proteins found in any species of protozoan.Chlorpheniramine: A histamine H1 antagonist used in allergic reactions, hay fever, rhinitis, urticaria, and asthma. It has also been used in veterinary applications. One of the most widely used of the classical antihistaminics, it generally causes less drowsiness and sedation than PROMETHAZINE.Mali: A country in western Africa, east of MAURITANIA and south of ALGERIA. Its capital is Bamako. From 1904-1920 it was known as Upper Senegal-Niger; prior to 1958, as French Sudan; 1958-1960 as the Sudanese Republic and 1959-1960 it joined Senegal in the Mali Federation. It became an independent republic in 1960.Quinine: An alkaloid derived from the bark of the cinchona tree. It is used as an antimalarial drug, and is the active ingredient in extracts of the cinchona that have been used for that purpose since before 1633. Quinine is also a mild antipyretic and analgesic and has been used in common cold preparations for that purpose. It was used commonly and as a bitter and flavoring agent, and is still useful for the treatment of babesiosis. Quinine is also useful in some muscular disorders, especially nocturnal leg cramps and myotonia congenita, because of its direct effects on muscle membrane and sodium channels. The mechanisms of its antimalarial effects are not well understood.Membrane Transport Proteins: Membrane proteins whose primary function is to facilitate the transport of molecules across a biological membrane. Included in this broad category are proteins involved in active transport (BIOLOGICAL TRANSPORT, ACTIVE), facilitated transport and ION CHANNELS.Sierra Leone: A republic in western Africa, south of GUINEA and west of LIBERIA. Its capital is Freetown.Mefloquine: A phospholipid-interacting antimalarial drug (ANTIMALARIALS). It is very effective against PLASMODIUM FALCIPARUM with very few side effects.Proguanil: A biguanide compound which metabolizes in the body to form cycloguanil, an anti-malaria agent.Treatment Failure: A measure of the quality of health care by assessment of unsuccessful results of management and procedures used in combating disease, in individual cases or series.Tanzania: A republic in eastern Africa, south of UGANDA and north of MOZAMBIQUE. Its capital is Dar es Salaam. It was formed in 1964 by a merger of the countries of TANGANYIKA and ZANZIBAR.Chemistry Techniques, Analytical: Methodologies used for the isolation, identification, detection, and quantitation of chemical substances.Treatment Outcome: Evaluation undertaken to assess the results or consequences of management and procedures used in combating disease in order to determine the efficacy, effectiveness, safety, and practicability of these interventions in individual cases or series.Dapsone: A sulfone active against a wide range of bacteria but mainly employed for its actions against MYCOBACTERIUM LEPRAE. Its mechanism of action is probably similar to that of the SULFONAMIDES which involves inhibition of folic acid synthesis in susceptible organisms. It is also used with PYRIMETHAMINE in the treatment of malaria. (From Martindale, The Extra Pharmacopoeia, 30th ed, p157-8)ColombiaMultidrug Resistance-Associated Proteins: A sequence-related subfamily of ATP-BINDING CASSETTE TRANSPORTERS that actively transport organic substrates. Although considered organic anion transporters, a subset of proteins in this family have also been shown to convey drug resistance to neutral organic drugs. Their cellular function may have clinical significance for CHEMOTHERAPY in that they transport a variety of ANTINEOPLASTIC AGENTS. Overexpression of proteins in this class by NEOPLASMS is considered a possible mechanism in the development of multidrug resistance (DRUG RESISTANCE, MULTIPLE). Although similar in function to P-GLYCOPROTEINS, the proteins in this class share little sequence homology to the p-glycoprotein family of proteins.Inhibitory Concentration 50: The concentration of a compound needed to reduce population growth of organisms, including eukaryotic cells, by 50% in vitro. Though often expressed to denote in vitro antibacterial activity, it is also used as a benchmark for cytotoxicity to eukaryotic cells in culture.Rwanda: A republic in eastern Africa, south of UGANDA, east of DEMOCRATIC REPUBLIC OF THE CONGO, west of TANZANIA. Its capital is Kigali. It was formerly part of the Belgian trust territory of Ruanda-Urund.QuinolinesKenya: A republic in eastern Africa, south of ETHIOPIA, west of SOMALIA with TANZANIA to its south, and coastline on the Indian Ocean. Its capital is Nairobi.Uganda: A republic in eastern Africa, south of SUDAN and west of KENYA. Its capital is Kampala.Papua New Guinea: A country consisting of the eastern half of the island of New Guinea and adjacent islands, including New Britain, New Ireland, the Admiralty Islands, and New Hanover in the Bismarck Archipelago; Bougainville and Buka in the northern Solomon Islands; the D'Entrecasteaux and Trobriand Islands; Woodlark (Murua) Island; and the Louisiade Archipelago. It became independent on September 16, 1975. Formerly, the southern part was the Australian Territory of Papua, and the northern part was the UN Trust Territory of New Guinea, administered by Australia. They were administratively merged in 1949 and named Papua and New Guinea, and renamed Papua New Guinea in 1971.Plasmodium vivax: A protozoan parasite that causes vivax malaria (MALARIA, VIVAX). This species is found almost everywhere malaria is endemic and is the only one that has a range extending into the temperate regions.NaphthyridinesMalaria, Vivax: Malaria caused by PLASMODIUM VIVAX. This form of malaria is less severe than MALARIA, FALCIPARUM, but there is a higher probability for relapses to occur. Febrile paroxysms often occur every other day.AfghanistanNigeria: A republic in western Africa, south of NIGER between BENIN and CAMEROON. Its capital is Abuja.

Relationships between malaria prevalence and malaria-related morbidity in school children from two villages in central Africa. (1/318)

To investigate the relationship between parasite prevalence and malaria-related morbidity, we carried out a comparative study among cohorts of school children from two villages, Dienga, Gabon, and Pouma, Cameroon, both located in malaria-endemic areas. Seven to 17 year-old children attending primary schools were similarly followed-up at each site to evaluate the frequency of malaria attacks. Follow-up involved daily temperature recording (and blood smears in the case of fever) and preparation of blood smears every two weeks. In Pouma, 186 children were followed-up for six months. In Dienga, 228 children were followed-up for nine months. The mean prevalence rate of Plasmodium falciparum infections (as assessed by the blood smears) was twice as high in Pouma compared with Dienga (45.2% versus 26.8%; P < 0.0001), whereas the monthly malaria attack rate (as assessed by the daily surveillance) was twice as high in Dienga compared with Pouma (21.5% versus 41.4%; P = 0.003). The possible implication of several parameters that may differ between the two areas, such as the malaria transmission level, the economical and social status of the inhabitants, the characteristics of infecting parasite strains, and the genetic background of the population, is discussed.  (+info)

Analysis of mefloquine resistance and amplification of pfmdr1 in multidrug-resistant Plasmodium falciparum isolates from Thailand. (2/318)

Resistance to quinoline-containing compound has been associated with the Plasmodium falciparum multidrug resistance 1 (pfmdr1) gene. We analyzed wild P. falciparum isolates with high levels of chloroquine and mefloquine resistance for their macrorestriction maps of chromosome 5 and sequence of pfmdr1. Two types of chromosome 5 amplification were found. Eleven of 62 resistant isolates displayed Bgl 1 fragments larger than 100 kb. Twenty-nine isolates possessed multiple copies of the fragments. We failed to detect any amplification of this region on chromosome 5 in 22 mefloquine-resistant isolates, suggesting that other mechanisms can mediate the mefloquine-resistant phenotype. There was no direct association between pfmdr1 mutations and chloroquine sensitivity. Resistant lines could have Asn-86 and Tyr-184 or Phe-184, the predicted sequence of those chloroquine-sensitive isolates. No mutation at Asn-1042 and Asp-1246 was detected among these chloroquine-resistant isolates. Therefore, a few base substitutions in the pfmdr1 gene may not be sufficient to account for all chloroquine-resistant phenotypes.  (+info)

Factors influencing resistance to reinfection with Plasmodium falciparum. (3/318)

A treatment-reinfection study design was used to investigate the relationships between host immunologic and/or genetic factors and resistance to reinfection with Plasmodium falciparum. Sixty-one children in Gabon were enrolled in a cross-sectional study to measure the prevalence of each human plasmodial species. All were given amodiaquine for radical cure of parasites, and 40 were subsequently followed-up for 30 weeks. Successive blood smears were examined to measure the delay of reappearance in blood of asexual stages of P. falciparum parasites. Presence of infection during the cross-sectional survey was associated with male sex, non-deficient glucose-6-phosphate dehydrogenase activity, plasma interleukin-10 level, and anti-LSA-Rep antibody concentration. Resistance to reinfection was related to the presence of anti-LSA-J antibodies, and the absence of anti-LSA-Rep antibodies. Moreover, P. malariae-infected subjects were usually co-infected with P. falciparum, and were also more rapidly reinfected with P. falciparum after treatment, compared with those without P. malariae infection.  (+info)

Antibiotics for prophylaxis of Plasmodium falciparum infections: in vitro activity of doxycycline against Senegalese isolates. (4/318)

The in vitro activities of doxycycline, chloroquine, quinine, amodiaquine, artemether, pyrimethamine, and cycloguanil were evaluated against Plasmodium falciparum isolates from Senegal (Dielmo and Ndiop), using an isotopic, micro, drug susceptibility test. The 71-50% inhibitory concentration (IC50) values for doxycycline ranged from 0.7 to 108.0 microM and the geometric mean IC50 for the 71 isolates was 11.3 microM (95% confidence interval = 9.5-13.4 microM). The activity of doxycycline did not differ significantly (P = 0.0858) between the chloroquine-susceptible isolates and the chloroquine-resistant isolates. There was no in vitro correlation between the responses to doxycycline and those to artemether, chloroquine, quinine, amodiaquine, pyrimethamine, and cycloguanil, suggesting no in vitro cross-resistance among these drugs. Potency was increased by prolonged exposure. In 96-hr incubations, the activity of doxycycline was 4-5-fold more increased than in 48-hr incubations. The in vitro activity of doxycycline against intraerythrocytic stages of multidrug-resistant P. falciparum, its action against the preerythrocytic forms, the lack of correlation between the responses in vitro of P. falciparum to doxycycline and the other antimalarial drugs, and its original potential site of action are factors that favor its use as antimalarial drug.  (+info)

In vivo efficacy study of amodiaquine and sulfadoxine/ pyrimethamine in Kibwezi, Kenya and Kigoma, Tanzania. (5/318)

We conducted two randomized clinical trials to determine the in vivo efficacy of amodiaquine and sulfadoxine/pyrimethamine in treating Plasmodium falciparum malaria. Seventy-five patients under the age of 10 years in Kibwezi, Kenya, and 171 patients in Kigoma, Tanzania, were enrolled for treatment. Due to loss of eight patients in Kibwezi and 37 in Kigoma to follow-up, we used best and worst case scenarios for the parasitological response. The in vivo sensitivity of Plasmodium falciparum to amodiaquine was 75% (no loss to follow-up) in Kibwezi and ranged from 85% in the best to 65% in the worst case scenario in Kigoma. The sensitivity to sulfadoxine/pyrimethamine was 70% to 88% in Kibwezi and 65% to 89% in Kigoma. R1 resistance to amodiaquine was 22% in Kibwezi and varied from 6% in the best to 26% for the worst case scenario in Kigoma. The R1 resistance to sulfadoxine/pyrimethamine was 5% to 23% in Kibwezi and 2% to 26% in Kigoma. R2 resistance was 3% for amodiaquine and 7% for sulfadoxine/pyrimethamine in Kibwezi and 9% in Kigoma for each treatment group. There was no statistically significant difference between treatment groups at either study site, except for a slight difference in R1 resistance in the best case scenario, Kibwezi, in favour of S/P. Although both amodiaquine and sulfadoxine/pyrimethamine resistance seems to be increasing, these antimalarials are still effective in parasite clearance.  (+info)

Adaptation of a chloroquine-resistant strain of Plasmodium vivax from Indonesia to New World monkeys. (6/318)

The spread of chloroquine-resistant Plasmodium vivax from Papua New Guinea and Indonesia poses a serious health threat to areas of Southeast Asia where this species of malaria parasite is endemic. A strain of P. vivax from Indonesia was adapted to develop in splenectomized Aotus lemurinus griseimembra, Aotus vociferans, Aotus nancymai, and Saimiri boliviensis monkeys. Transmission to splenectomized Saimiri monkeys was obtained via sporozoites. Chemotherapeutic studies indicated that the strain was resistant to chloroquine and amodiaquine while sensitive to mefloquine. Infections of chloroquine-resistant P.vivax in New World monkeys should be useful for the development of alternative treatments.  (+info)

Role of extraneuronal mechanisms in the termination of contractile responses to amines in vascular tissue. (7/318)

1 The role of the uptake and release of agonist from extraneuronal sites in the termination of responses of rabbit aortic strips to amines was studied. 2 Strips were contracted with adrenaline or noradrenaline and after response plateau was reached, the muscle chambers were washed free of agonist and the relaxation in Krebs solution recorded. After inhibition of catechol-O-methyl-transferase, monoamine oxidase and neuronal uptake the relaxation rate was greatly prolonged. Evidence is provided that this very slow relaxation resulted from the accumulation of intact amine at extraneuronal sites during exposure to the agonist and its subsequent release past receptors due to a reversal of the concentration gradient after washout. 3 Pretreatment with the haloalkylamine, GD-131 (N-cyclohexylmethyl-N-ethyl-beta-chloroethylamine), an inhibitor of extraneuronal uptake, returned the slow relaxation rate after enzyme inhibition towards that of control strips. By blocking the extraneuronal transport of amines their accumulation at intracellular loci after enzyme inhibition was prevented. 4 The effects of GD-131 and 17beta-oestradiol on the relaxation rate of untreated strips contracted by adrenaline and noradrenaline confirmed that extraneuronal uptake to sites of enzymatic activity is the major mechanism terminating their action. 5 Inactivation of extraneuronal transport sites by GD-131 was prevented by protecting them with 17beta-oestradiol or normetanephrine during exposure to the haloalkylamine, pointing to a common site of action of these agents on a specific carrier system for amines. 6 Evidence is presented that the relaxation from contractions induced by histamine and 5-hydroxytryptamine also involves extraneuronal accumulation and release, probably by an uptake process which is identical to the one for catecholamines.  (+info)

"One-pot" synthesis and antimalarial activity of formamidine derivatives of 4-anilinoquinoline. (8/318)

Amodiaquine (AQ) is an antimalarial which is effective against chloroquino-resistant strains of Plasmodium falciparum but whose clinical use is severely restricted because of associated hepatotoxicity and agranulocytosis. "One-pot" synthesis of formamidines likely to be transformed into AQ derivatives is reported. Compared with AQ, the new compounds were devoid of in vitro cytotoxicity upon human embryonic lung cells and mouse peritoneal macrophages. One showed a potent in vivo activity in mice infected with P berghei. Transformation of this compound by reductive amination led to a new type of AQ derivatives that displayed an in vitro activity similar to that of AQ but did not lead to toxic quinone-imines.  (+info)

Abstract The antimalarial activities of amodiaquine, the desethyl metabolite of amodiaquine, chloroquine, and mefloquine were evaluated against 35 field isolates of Plasmodium falciparum collected from eastern Thailand, October-December 1985, to define patterns of cross-resistance among these compounds. The assay system was based on the in vitro inhibition of schizont maturation. The parasites were generally sensitive to mefloquine (mean 50%-inhibitory concentrations = 9.98 nM) and highly resistant to chloroquine (IC50 = 313 nM). The mean in vitro activity of desethylamodiaquine (67.5 nM) was approximately 3.5 times lower than that of amodiaquine (18.2 nM). There was a significant rank-order correlation between the IC50s of desethylamodiaquine and chloroquine, but not between amodiaquine and chloroquine, which suggests that the apparent cross-resistance between chloroquine and amodiaquine observed in clinical studies may be more closely related to the cross-resistance between chloroquine and the
Mutations in the Plasmodium falciparum genes pfcrt and pfmdr1 are selected by amodiaquine treatment in Africa. To examine the importance of these mutations in amodiaquine-treated Asian parasites, we determined pre- and posttreatment genotypes for amodiaquine treatment failures from a clinical trial in Afghanistan. The pfcrt codon 72 to 76 haplotype SVMNT was present in all samples tested, both before and after treatment. Amodiaquine did not clearly select for any pfmdr1 genotype, but a novel mutation, pfmdr1 N86F, was detected in four samples. We provide in vivo data to support the in vitro correlation between pfcrt SVMNT and increased resistance to the metabolite of amodiaquine.,br/, ...
Background: The development and spread of antimalarial drug resistant parasites contributes to the global impact of the disease. In vivo efficacy assessments of treatments for Plasmodium falciparum malaria are essential for ensuring effective case management. Artemisinin-based combinations have been adopted as the first-line treatment for uncomplicated P. falciparum malaria in Cameroon since 2004. Methods: A total of 177 children aged six-months to 10 years with uncomplicated mono-infected falciparum malaria were randomized (1:1) to receive artesunate/sulphadoxine-pyrimethamine (AS/SP) or artesunate/amodiaquine (AS/AQ) pediatric tablets and followed up for 28 days according to the standard World Health Organization in vivo drug efficacy monitoring protocol. The primary and secondary endpoints were PCR uncorrected and corrected cure rates, as measured by adequate clinical and parasitological response (ACPR) on day 28. Results: The PCR corrected cure rate was high, overall (88.1%, 95% CI 83.1-93.1), 85.9%
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Main results: 56 studies included, mostly from Africa. Treatment allocation was adequately concealed in three trials, and unclear or inadequate in the remainder. Amodiaquine was more effective than chloroquine for parasite clearance (day 7, Peto odds ratio 4.42 (95% confidence interval 3.65 to 5.35); day 14, Peto odds ratio 6.44 (95% confidence interval (CI) 5.09 to 8.15). Comparisons with sulfadoxine/pyrimethamine were more mixed, with sulfadoxine/pyrimethamine more effective on day 28 (Peto odds ratio 0.41; 95% CI 0.28 to 0.61). No significant difference for adverse events was observed between amodiaquine and chloroquine and sulfadoxine/pyrimethamine. Reported adverse effects were minor or moderate. No life threatening events were detected ...
Abstract. Home management of malaria is recommended for prompt, effective antimalarial treatment in children less than five years of age. Compliance, safety, and effectiveness of the new fixed-dose artesunate-amodiaquine regimen used to treat suspected malaria were assessed in febrile children enrolled in a 24-month cohort study in two settings in Madagascar. Children with fever were asked to visit community health workers. Presumptive antimalarial treatment was given and further visits were scheduled for follow-up. The primary endpoint was the risk of clinical/parasitologic treatment failure. Secondary outcomes included fever/parasite clearance, change in hemoglobin levels, and frequency of adverse events. The global clinical cure rate was 98.4% by day 28 and 97.9% by day 42. Reported compliance was 83.4%. No severe adverse effects were observed. This study provides comprehensive data concerning the clinical cure rate obtained with artesunate-amodiaquine and evidence supporting the scaling up of home
CD4+ T cells play key roles in the regulation of immune responses against pathogenic infectious antigens via development into effector T helper and induced regulatory T (iTreg) cells. Particularly, CD4+CD25+Foxp3+ iTreg cells are crucial for maintaining immune homeostasis and controlling inflammatory diseases. Anti-inflammatory drugs that enhance iTreg cell generation would be effective at preventing and treating inflammatory and autoimmune diseases. In this study, we examined whether anti-malarial and anti-arthritic amodiaquine (AQ) could affect iTreg cell development. Despite the anti-proliferative activity of AQ, AQ only moderately decreased iTreg cell proliferation but substantially increased IL-2 production by iTreg cells. Furthermore, AQ dose-dependently increased iTreg cell development and significantly upregulated iTreg cell markers including CD25. Interestingly, CD25 expression was decreased at later stages of iTreg cell development but was sustained in the presence of AQ, which was ...
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Artesunate-amodiaquine (AS-AQ) is one of the most widely used artemisinin-based combination therapies (ACTs) to treat uncomplicated Plasmodium falciparum malaria in Africa. We investigated the impact of different dosing strategies on the efficacy of this combination for the treatment of falciparum malaria. Individual patient data from AS-AQ clinical trials were pooled using the WorldWide Antimalarial Resistance Network (WWARN) standardised methodology. Risk factors for treatment failure were identified using a Cox regression model with shared frailty across study sites. Forty-three studies representing 9,106 treatments from 1999-2012 were included in the analysis; 4,138 (45.4%) treatments were with a fixed dose combination with an AQ target dose of 30 mg/kg (FDC), 1,293 (14.2%) with a non-fixed dose combination with an AQ target dose of 25 mg/kg (loose NFDC-25), 2,418 (26.6%) with a non-fixed dose combination with an AQ target dose of 30 mg/kg (loose NFDC-30), and the remaining 1,257 (13.8%) with a co
The study discuss the potential impact of seasonal malaria chemoprevention (SMC) on the cases of malaria, anaemia and molecular markers resistance Plasmodium falciparum malaria; and also review the mechanism of action and the effect on immunity of SMC. SMC using an efficacious drug is likely to substantially reduce cases of clinical malaria in high transmission settings. However, an increase of molecular markers could hamper rolling out SMC as a national policy.   Key words: Seasonal malaria chemoprevention impact, malaria molecular markers, review.  
Without an effective vaccine for the prevention of malaria, a fundamental component of the strategy for the control of this disease is based on prompt and effective treatment. Due to the high resistance level of Plasmodium falciparum to the most affordable drugs such as chloroquine and sulfadoxine-pyrimethamine, artemisinin-based combination therapies are presently used in many countries or are being developed for registration. One artemisinin combination therapy that is drawing a certain degree of interest is the combination of artesunate (a short half-life drug) plus amodiaquine (a long half-life drug that is presently used in loose combination in many countries). The short half-life drug achieves substantial and rapid parasite killing, while a high concentration of the long half-life drug kills off the remaining malaria parasites. In addition to the effectiveness of 3 days of treatment (rapid clearance of fever and malaria parasites) in western and central Africa, where resistance to ...
Quick Search Product Directory Listing in Alphabetical IndexA on Drugdu.com for Artemether and Lumefantrine Tablets|||269315|||astra-lifecare-india-pvt, Amodiaquine HCl Tablets USP 200 mg|||269313|||astra-lifecare-india-pvt, Aciclovir Tablets BP 200 mg|||269307|||astra-lifecare-india-pvt and more.
The orphan nuclear receptor Nurr1 is ascribed high potential as molecular target for Parkinsons Disease and Alzheimers Disease treatment1,2 but small molecule Nurr1 ligands and mechanistic understanding of Nurr1 modulation are scarce.. Inspired by a PDB-deposited X-ray structure of Nurr1 in complex with the arachidonic acid metabolite prostaglandin A13, we hypothesized non-steroidal anti-inflammatory drugs (NSAIDs) as Nurr1 ligands. Screening of a structurally diverse collection of NSAIDs indeed discovered several Nurr1 modulators most of which, interestingly, exhibited inverse agonism on Nurr1. Together with the previously reported Nurr1 agonist amodiaquine4, these molecules add up to a set of initial tool compounds, i.e. parecoxib, oxaprozin, amodiaquine and chloroquine, to decipher the molecular function of Nurr1.. Using this initial tool, we probed the response of the Nurr1 ligand binding domain to modulation by ligands. We observed an ability of Nurr1 agonists to stimulate homo- and ...
The mainland Chinese started studying the anti-malarial effects of the traditional anti-malarial medicine derived from the plant Artemisa anna back in the 1960s. For various reasons, including the upheavals of the Cultural Revolution, the positive results were not published internationally. When they were, in the 1990s, they were pretty much "poohed-poohed" by the developed world except … the pharmaceuticals who pricked up their ears and went for it big time! The plants active ingredient was Artemisin and soon the synthetic Artesunate was developed.. Artesunate is fast-acting but has a very short half-life (i.e. very quickly disappears from the blood). Amodiaquine has longer half-life. The tablets are marketed in packs of a pair a day. If there is still some residual malaria, then a second line of attack is used - the trade name Coartem, a combination of Artesunate and Lumefantrine (in turn developed from halofantrine, the basis of Halfan, which at the time of its recent development was ...
Calcium, Concentration, Graphene, Nanoribbon, Paper, Drugs, Role, Lead, Bath, Cymbopogon, Endothelium, Indomethacin, Muscle, Phenylephrine, Prostacyclin, Relaxation, Smooth Muscle, Tissue, Vascular Smooth Muscle, Amodiaquine
Assuming the following reaction proceeds in the forward direction, 3 Sn4+(aq) + 2 Cr(s)  3 Sn2+(aq) + 2 Cr3+(aq) a. Sn4+(aq) is the reducing agent and Cr(s) is the oxidizing agent. b. Cr(s) is the reducing agent and Sn2+(aq ...
BACKGROUND: The emergence of resistance against artemisinin combination treatment is a major concern for malaria control. ACTs are recommended as the rescue treatment, however, there is limited evidence as to whether treatment and re-treatment with ACTs select for drug-resistant P. falciparum parasites. Thus, the purpose of the present study is to investigate the impact of (re-)treatment using artesunate-amodiaquine (ASAQ) and artemether-lumefantrine (AL) on the selection of P. falciparum multidrug resistance-1 (Pfmdr1) alleles in clinical settings.. METHODS: P. falciparum positive samples were collected from children aged 12-59 months in a clinical trial in DR Congo and Uganda. Pfmdr1 single nucleotide polymorphisms (SNPs) analysis at codons N86Y, Y184F, and D1246Y were performed at baseline and post-treatment with either AL or ASAQ as a rescue treatment using nested PCR followed by restriction fragment length polymorphism (RFLP) assays.. RESULTS: The pre-treatment prevalence of Pfmdr1 N86 and ...
This study evaluated and compared the efficacy of five brands of Artemisinin Combination Therapies (ACTs); Dihydroartemisinin plus Piperaquine, Artesunate plus Amodiaquine, Artesunate plus Sulphadoxine/Pyrimethamine, Artemether plus lumefantrine and Artesunate plus mefloquine combinations in vivo in P.berghei infected swiss albino mice. The experimental animals were pre-screened to rule out infection. All drugs were administered as clinical doses for the curative test and the Mean Percentage Parasitemia level assessed daily for seven days and on day 60. The results showed that all the drugs were effective with artesunate plus amodiaquine combination being the most efficacious followed by dihydroartemisinin plus piperaquine and artesunate plus sulphadoxine plus pyrimethamine combinations followed by artesunate plus mefloquine combination and artemether plus lumefantrine combination which was the least efficacious. Results on day 60 showed increasing parasitemia levels in mice which received Artemether
Significant interest has been placed on the utility of PK parameters in predicting the treatment response. Most attention has been placed on the correlates of the AUC, as AUC represents both the duration and the degree of exposure. The accurate measurement of AUC in field studies is difficult, so recent efforts for studying the PKs of artemisinin partner drugs have focused on single day 7 drug levels (34). The rationale for this approach is that by day 7 the remaining parasites will be exposed only to the partner drug, as the rapidly eliminated artemisinin derivatives are no longer present. The level of partner drug in the days following dosing may be critical for determining both the clearance of the infection and the potential selection of drug-resistant parasites. Importantly, for the longer-acting partner drugs, the day 7 levels appear to correlate with the AUC (5), as seen for both DEAQ and LR in our study. Several studies from Thailand have examined the relationship between the day 7 ...
Bulk Pharmaceuticals Acyclovir CAS 59277-89-3 Albendazole CAS 54965-21-8 Allopurinol CAS 315-30-0 Alpha Methyldopa CAS 555-30-6 Amodiaquine CAS 86-42-0 Amprolium HCL CAS 121-25-5 Analgin CAS
Find out how to take Artesunate (drug) and its dose. Describes the best time to take the drug and precautions if any that should be followed.
Afin daider à lidentification des enzymes, les codes IUPAC sont donnés en note pour chacune delles; utiliser si possible un descripteur plus spécifique (fr) ...
BACKGROUND: Gametocytes are responsible for transmission of malaria from human to mosquito. Artemisinin combination therapy (ACT) reduces post-treatment gametocyte carriage, dependent upon host, parasite and pharmacodynamic factors. The gametocytocidal properties of antimalarial drugs are important for malaria elimination efforts. An individual patient clinical data meta-analysis was undertaken to identify the determinants of gametocyte carriage and the comparative effects of four ACTs: artemether-lumefantrine (AL), artesunate/amodiaquine (AS-AQ), artesunate/mefloquine (AS-MQ), and dihydroartemisinin-piperaquine (DP). METHODS: Factors associated with gametocytaemia prior to, and following, ACT treatment were identified in multivariable logistic or Cox regression analysis with random effects. All relevant studies were identified through a systematic review of PubMed. Risk of bias was evaluated based on study design, methodology, and missing data. RESULTS: The systematic review identified 169 published
The World Health Organization recommends the use of artemisinin-based combination therapy (ACT) to treat uncomplicated malaria for the control of malaria across the world. There are several types of ACT used across malaria-endemic countries, yet there is little information about preferences and adherence practices regarding different types of ACT. The objective of this study was to evaluate levels of adherence to two types of ACT, artemether-lumefantrine (AL) and artesunate + amodiaquine (ASAQ), for the treatment of uncomplicated malaria among prescribers and patients in Guinea in 2016. The study included a review of records of malaria patients and three health-facility, cross-sectional surveys. Patients diagnosed with uncomplicated malaria and prescribed ACT (n = 1830) were recruited and visited in their home after receiving the medication and administered a questionnaire regarding ACT adherence. Prescribers (n = 115) and drug dispensers (n = 43) were recruited at the same public health facilities and
Malaria continues to be one of the leading killer diseases in the tropical areas affecting the world's poorest children and pregnant women and resista...
Sulfalene and sulfadoxine are folic acid antagonists which inhibit a Plasmodium- close to that of sulfadoxine and it therefore specifi c enzyme, dihydropteroate-synthase seems reasonable to combine sulfalene/(DHPS). These drugs bind protein strongly pyrimethamine with amodiaquine since and have relatively long half-lives (65 and it has been shown that a combination of 180 hours respectively)14. Sulfalene/pyrimethamine has not been used is more effective than either product on its for over three decades and, as a result, it is likely own, and that its safety profi le is identical that todays plasmodia have not been subjected to selection pressure from this combination pyrimethamine. In 2002 (before PCR) in and have remained maximally sensitive. Uganda, Talisuna et al. (10) recorded a Since amodiaquine remains effective (15), we parasitologic effi cacy rate of 85.7%, and in organised a study to compare the combinations Rwanda in 2001, Rwagacondo et al.16 obtained ...
There is hope that none of the above-mentioned concerns will be substantiated in larger, upcoming trials. What can be done besides hoping? Attempts to regain efficacy of artemisinins by increasing dose were disappointing [24] and since only fixed-dose combinations are licensed, increased partner drug dosing could be associated with increased toxicity and adherence issues. Extending the course of routine 3-day treatment to 5 or 7 days was successful, associated with a cure rate of 98% in western Cambodia, the epicentre of drug resistance [25]. The cost of such compromised regimens will increase, while adherence could decrease. Practitioners in Vietnam have instead empirically started to add mefloquine to the current DHA-piperaquine first-line treatment. There appears to be an inverse susceptibility between piperaquine and mefloquine. A similar inverse susceptibility between co-artemether (artemether/lumefantrine) and amodiaquine could be exploited as stopgap measure in Africa [26]. Mefloquine did ...
HIV and malaria are two of the most pernicious diseases facing developing countries. Malaria affects 300 to 500 million individuals annually in developing countries and it is estimated that 25.8 million people in Africa live with HIV. Current therapy recommended by the World Health Organization includes the use of artemisinin derivatives, such as artesunate and artemether. To minimize the risk of resistance, these drugs are used in combination with older drugs with longer half-lives including amodiaquine and lumefantrine.. Treatment of malaria is further complicated by the increasing availability of antiretroviral (ARV) medications for HIV in that clinically important drug-drug interactions may occur in co-infected patients. Protease inhibitor (e.g. lopinavir and ritonavir) and non-nucleoside reverse transcriptase (e.g. efavirenz) based treatment commonly affects pharmacokinetic exposure of drugs metabolized by cytochrome P450 (CYP) metabolic pathways.. Artemether is metabolized by the CYP3A4 to ...
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Amodiaquine is a potent, non-competitive inhibitor of histamine N-methyl transferase in human erythrocytes, also used as an antimalarial and anti-inflammatory agent. Buy Histone Methyltransferase inhibitor Amodiaquin dihydrochloride dihydrate from AbMole BioScience.
En Belgique, INEOS est composé de plusieurs succursales qui disposent à leur tour de plusieurs sociétés. Ces sociétés appartiennent aux différentes divisions au sein du group INEOS.. Les mêmes conditions dachat sont valable pour toutes nos succursales. Vous pouvez les télécharger ci-dessous.. INEOS Conditions dachat INEOS Life Saving Rules. Des informations plus spécifiques sont disponibles en cliquant sur une des succursales ci-dessous.. ...
|p|AQ is a bio-product made of natural ingredients. Designed to eradicate bacteria and viruses in air and any surfaces to radically enhance indoor and personal hygiene. Unlike its chemical counterpart, the bio-structure of AQ is far too complicated to be
Detailed dosage guidelines and administration information for Follistim AQ (follitropin). Includes dose adjustments, warnings and precautions.
Artemisinin-based combination therapy (ACT) is used extensively as first-line treatment for uncomplicated falciparum malaria. There has been no rigorous assessment of the potential for racial/ethnic differences in the pharmacokinetic properties of ACTs that might influence their efficacy. Areas covered: A comprehensive literature search was performed that identified 72 publications in which the geographical origin of the patients could be ascertained and the key pharmacokinetic parameters maximum drug concentration (Cmax), area under the plasma concentration-time curve (AUC) and elimination half-life (t½β) were available for one or more of the five WHO-recommended ACTs (artemether-lumefantrine, artesunate-amodiaquine, artesunate-mefloquine, dihydroartemisinin-piperaquine and artesunate-sulfadoxine-pyrimethamine ...
Seasonal malaria chemoprevention (SMC) was recommended in 2012 for young children in the Sahel during the peak malaria transmission season. Children are given a single dose of sulfadoxine/pyrimethamine combined with a 3-day course of amodiaquine, once a month for up to 4 months. Roll-out and scale-up of SMC has been impressive, with 12 million children receiving the intervention in 2016. There is evidence of its overall benefit in routine implementation settings, and a meta-analysis of clinical trial data showed a 75% decrease in clinical malaria compared to placebo. SMC is not free of shortcomings. Its target zone includes many hard-to-reach areas, both because of poor infrastructure and because of political instability. Treatment adherence to a 3-day course of preventive treatment has not been fully documented, and could prove challenging. As SMC is scaled up, integration into a broader, community-based paradigm which includes other preventive and curative activities may prove beneficial, both ...
Over-diagnosis of malaria among African children results in mismanagement of non-malaria infections. Limited laboratory capacity makes it difficult to implement policies that recommend pre-treatment confirmation of infections so a new approach with a package for on-the-spot management of fevers was evaluated. Febrile children presenting to outpatient clinic were randomized to receive either a test-treat package (history with clinical examination; point-of-care tests; choice of artesunate-amodiaquine, co-amoxiclav and/or paracetamol) or routine outpatient care in a secondary health care facility in Kumasi, Ghana. A diagnosis of malaria, bacterial, viral or mixed malarial and bacterial infections was made using pre-defined criteria. Outcome was resolution of all symptoms including fever on day 7. The median age of the patients was 37.5 months (IQR: 19 to 66 months), with 56.7% being males. Compared to routine care the test-treat package resulted in less diagnoses of malaria, (37.2% vs 46.2%, p = ...
Seven patients developed hepatitis after receiving amodiaquine for malaria prophylaxis for 4 to 15 weeks. Four patients had a minor form of hepatitis: jaundice was mild or absent, serum aminotransferase levels were moderately increased, and recovery was prompt. Three patients had a severe form: jaundice was intense, serum aminotransferase levels were markedly increased, jaundice persisted for 3 to 6 months, and liver tests were still abnormal 7 to 27 months after the onset of hepatitis. In two patients, serum aminotransferase levels increased promptly after readministration of the drug, which is consistent with an immunoallergic mechanism for amodiaquine-induced hepatitis. ...
<p>An outline of the opportunities and challenges in large-scale use of artemisinin combination therapies to treat malaria.</p>
21 6 Fe 2+ (aq) 6 Fe 3+ (aq) + 6 e - 6 Fe 2+ (aq)  6 Fe 3+ (aq) + 6 e - Cr 2 O 7 2- (aq) + 6 e - 2 Cr 3+ (aq) Cr 2 O 7 2- (aq) + 6 e -  2 Cr 3+ (aq) 6 Fe 2+ (aq) + Cr 2 O 7 2- (aq) + ? 2nd H + (aq) 6 Fe 3+ (aq) + 2 Cr 3+ (aq) + ? 1st Oxygen H 2 O (l) 6 Fe 2+ (aq) + Cr 2 O 7 2- (aq) + ? 2nd H + (aq)  6 Fe 3+ (aq) + 2 Cr 3+ (aq) + ? 1st Oxygen H 2 O (l) Oxygen = 7 2nd (Hydrogen) = 14 Balancing Redox Equations in acidic solutions ...
Data for artesunate, used for the treatment of malaria, indicates IVC in conjunction with IV Artesunate makes a substantial difference in advanced cancers.
Get an answer for Calculate Kc for the system, Ni2+ + Co Ni + Co2+. at 25 C?Ni2+ (aq) + 2e === Ni (s) E = - 0.25 V Co2+ (aq) + 2e === Co (s) E = - 0.28 and find homework help for other Science questions at eNotes
Determine the potential of each of the following cells: a) Pt(s) / H2(g,1.0 bar) / HCl(aq, 0.075 M) // HCl(aq, 1.0M) / H2(g, 1.0 bar) /Pt(s) In the solutions manual, they give the balanced equation as: 2H+ (aq, 1.0M) + H2(g, 1 atm) ----, 2H+ (aq, 0.075M) + H2 (g, 1 atm) If you go on to calculate E(c ...
The [H3O+] of a solution with pH = 3 is -10 M. 10 M. 1 x 10-3 M. 1 x 103 M. 1 x 10-11 M. Identify the acid(s) and base(s) in the following reaction: CH3COOH(aq) + NH3(aq) CH 3COO-(aq) + NH4+(aq) CH3COOH is the only acid, and NH3 is ...
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Comparison of regimen efficacy in clinical medicine has been utilized to improve the effect of drugs against disease The pairs alternative t-test meth..
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We produce Dihydroartemisinin + Piperaquine Phosphate Tablets and other Antimalarial drugs in the following forms: -Artemether (Injection, Tablets) -Artesunate + Amodiaquine (Tablets) -Artesunate + Mefloquine HCL (Tablets) -Artesunate + .....
Our Molecular Group provides tools that summarise the prevalence of molecular markers for resistance to artemisinin, chloroquine, lumefantrine, amodiaquine and sulfadoxine-pyrimethamine and displays the patterns of these markers by location and time to facilitate management and containment of antimalarial resistance
Malaria, Plasmodium, Plasmodium Falciparum, Gold, Administration, Amodiaquine, Evaluation, Falciparum Malaria, Mefloquine, Parasites, Patients, Primaquine, Pyrimethamine, Sulfadoxine, Time, Treatment, Treatments, Health, Hospitals, Infection
BACKGROUND: Use of different methods for assessing the efficacy of artemisinin-based combination antimalarial treatments (ACTs) will result in different estimates being reported, with implications for changes in treatment policy. METHODS: Data from different in vivo studies of ACT treatment of uncomplicated falciparum malaria were combined in a single database. Efficacy at day 28 corrected by PCR genotyping was estimated using four methods. In the first two methods, failure rates were calculated as proportions with either (1a) reinfections excluded from the analysis (standard WHO per-protocol analysis) or (1b) reinfections considered as treatment successes. In the second two methods, failure rates were estimated using the Kaplan-Meier product limit formula using either (2a) WHO (2001) definitions of failure, or (2b) failure defined using parasitological criteria only. RESULTS: Data analysed represented 2926 patients from 17 studies in nine African countries. Three ACTs were studied: ...
Examples include amodiaquine, chloroquine, and hydroxychloroquine. Amodiaquine Chloroquine Hydroxychloroquine Bray PG, Hawley ... SR, Ward SA (1996). "4-Aminoquinoline resistance of Plasmodium falciparum: insights from the study of amodiaquine uptake". Mol ...
... is a benzamide,[12] derivative of morpholine,[103] which acts pharmacologically as a selective, reversible inhibitor of monoamine oxidase A (RIMA),[9] a type of monoamine oxidase inhibitor (MAOI), and increases levels of norepinephrine (noradrenaline), dopamine, and especially serotonin.[104][105] in neuronal cells as well as in synaptic vesicles; extracellular levels also increase which results in increased monoamine receptor stimulation and suppression of REM sleep, down regulation of 3-adrenoceptors. A single 300 mg dose of moclobemide inhibits 80% of monoamine oxidase A (MAO-A) and 30% of monoamine oxidase B (MAO-B), blocking the decomposition of norepinephrine, serotonin and, to a lesser extent, dopamine. There is also some evidence pointing towards moclobemide possessing neuroprotective properties.[8] There is no cumulative effect of moclobemide centrally when taken long-term.[8] With long-term use of moclobemide, there is a significant down-regulation of B-adrenoceptors.[8] ...
... (CHF-3381, V-3381) is a drug which was formerly being investigated as an anticonvulsant and neuroprotective and is now under development for the treatment of neuropathic pain and chronic cough in Europe by Vernalis and Chiesi.[1][2][3][4][5][6][7][8] It acts as a competitive, reversible, and non-selective monoamine oxidase inhibitor,[5][6][9] and as a low affinity, non-competitive NMDA receptor antagonist.[1][2][10] A pilot study of indantadol for chronic cough was initiated in October 2009 and in April 2010 it failed to achieve significant efficacy in neuropathic pain in phase IIb clinical trials.[7][8][11][12] ...
... , a pathway inhibitor in the synthesis of the neurotransmitter dopamine, was used to determine the effects of decreased dopamine levels in social spacing of Drosophila melanogaster. 3-4 day old flies that were fed 3-iodotyrosine for 24 hours were shown to have altered dopamine levels.[3] ...
A deficiency of tyrosine hydroxylase leads to impaired synthesis of dopamine as well as epinephrine and norepinephrine. It is represented by a progressive encephalopathy and poor prognosis. Clinical features include dystonia that is minimally or nonresponsive to levodopa, extrapyramidal symptoms, ptosis, miosis, and postural hypotension. This is a progressive and often lethal disorder, which can be improved but not cured by levodopa.[39] Response to treatment is variable and the long-term and functional outcome is unknown. To provide a basis for improving the understanding of the epidemiology, genotype/phenotype correlation and outcome of these diseases their impact on the quality of life of patients, and for evaluating diagnostic and therapeutic strategies a patient registry was established by the noncommercial International Working Group on Neurotransmitter Related Disorders (iNTD).[40] Additionally alterations in the tyrosine hydroxylase enzyme activity may be involved in disorders such as ...
Delini-Stula, A.; Fischbach, R.; Gnirss, F.; Bures, E.; Pöldinger, W. (1985). "Early experience with CGP 4718 A (Sercloremine), a new selective and reversible MAO-A and 5-HT-uptake inhibitor, in the treatment of depressive patients". Drug Development Research. 6 (4): 371-384. doi:10.1002/ddr.430060409. ISSN 0272-4391 ...
... is an alkaloid found in Corydalis (Papaveraceae) and Dicentra, plants in the family Fumariaceae that can cause fatal poisoning in sheep and cattle.[citation needed] It has been shown to act as an acetylcholinesterase inhibitor,[1] and inhibits biosynthesis of dopamine via inhibition of the enzyme tyrosine hydroxylase.[2][3] Like apomorphine, it is reported to be an inhibitor of amyloid beta protein (Aβ) fiber formation, whose presence is a hallmark of Alzheimer's disease (AD). Bulbocapnine is thus a potential therapeutic under the amyloid hypothesis.[4] According to the Dorlands Medical Dictionary, it "inhibits the reflex and motor activities of striated muscle. It has been used in the treatment of muscular tremors and vestibular nystagmus".[5] A psychiatrist at Tulane University named Robert Heath carried out experiments on prisoners at the Louisiana State Penitentiary using bulbocapnine to induce stupor.[6] This work at Tulane inspired, and was continued parallel to, experiments ...
Chloroquine Amodiaquine Pamaquine Mefloquine Drugs.com: Quinacrine. Retrieved on August 24, 2009. Toubi E, Kessel A, Rosner I, ...
... was also the first drug used for treatment of malaria.[40] Quinine was used as a muscle relaxant by the Quechua, who are indigenous to Peru, Bolivia and Ecuador, to halt shivering due to low temperatures.[41] The Quechuas would mix the ground bark of cinchona trees with sweetened water to offset the bark's bitter taste, thus producing tonic water.[citation needed] The Jesuits were the first to bring cinchona to Europe. The Spanish were aware of the medicinal properties of cinchona bark by the 1570s or earlier: Nicolás Monardes (1571) and Juan Fragoso (1572) both described a tree that was subsequently identified as the cinchona tree and whose bark was used to produce a drink to treat diarrhea.[42] Quinine has been used in unextracted form by Europeans since at least the early 17th century. It was first used to treat malaria in Rome in 1631. During the 17th century, malaria was endemic to the swamps and marshes surrounding the city of Rome. Malaria was responsible for the deaths of ...
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Coartem is provided without profit to developing countries using grants from the Global Fund to Fight AIDS, Tuberculosis and Malaria, US President's Malaria Initiative along with other donors. Novartis has lowered the price of Coartem by 50% since 2001, increasing access to patients around the world. The first significant price reduction occurred in 2006, when the price of Coartem decreased from an average of US $1.57 to US $1.00. In 2006, due to an improved supply situation for the natural ingredient artemisinin, Novartis was able to undertake the pharmaceutical industry's most aggressive manufacturing scale-up of its kind from 4 million treatments in 2004 to 62 million treatments in 2006.[citation needed] Novartis and its partners invested heavily in expanding production capacity at their facilities in China, and Suffern, New York. This increase in production capacity ensured that supplies of Coartem met demand which enabled Novartis to further decrease the price of Coartem. In April 2008, ...
... is a form of aminoquinoline with an amine at the 8-position of quinoline. The 8-aminoquinoline family of drugs contains three members, primaquine, tafenoquine and pamaquine[1] and are used in the treatment of malaria. They may be used to eradicate malaria hypnozoites from the liver and have both been used for malaria prophylaxis. The 8-aminoquinoline drugs must not be given to patients with G6PD deficiency, because they cause potentially fatal haemolysis in these patients. Pamaquine is no longer available anywhere, but primaquine is still used routinely worldwide as part of the treatment of Plasmodium vivax and Plasmodium ovale malaria. Tafenoquine is currently in Phase III clinical trials and is not yet available to prescribe. ...
... is primarily used to prevent relapse of malaria due to Plasmodium vivax and Plasmodium ovale.[9] It eliminates hypnozoites, the dormant liver form of the parasite,[10] after the organisms have been cleared from the bloodstream.[9] If primaquine is not administered to patients with proven P. vivax or P. ovale infection, a very high likelihood of relapse exists for weeks or months (sometimes years).[9] Use in combination with quinine or chloroquine each of which is very effective at clearing P. vivax from blood, improves outcomes; they appear to also potentiate the action of primaquine.[11] As of 2016, the Centers for Disease Control and Prevention recommended the use of primaquine for primary prophylaxis prior to travel to areas with a high incidence of P. vivax, and for terminal prophylaxis (anti-relapse therapy) after travel.[4] A single dose of primaquine has rapid and potent ability to kill gametocytes (stage V) of P. falciparum and P. vivax in blood; it also kills asexual ...
... was formulated at Walter Reed Army Institute of Research (WRAIR) in the 1970s shortly after the end of the Vietnam war. Mefloquine was number 142,490 of a total of 250,000 antimalarial compounds screened during the study.[3] Mefloquine was the first Public-Private Venture (PPV) between the US Department of Defense and a pharmaceutical company. WRAIR transferred all its phase I and phase II clinical trial data to Hoffman LaRoche and Smith Kline. FDA approval as a treatment for malaria was swift. Most notably, phase III safety and tolerability trials were skipped.[3] The drug was first approved and sold on a commercial basis in Switzerland in 1985.[31] However, mefloquine was not approved by the FDA for prophylactic use until 1989. This approval was based primarily on compliance, while safety and tolerability were overlooked.[3] Because of the drug's very long half-life, the Centers for Disease Control originally recommended a mefloquine dosage of 250 mg every two weeks; however, this ...
"Artesunate Amodiaquine Winthrop (artesunate, amodiaquine) [summary of product characteristics]" (PDF). Sanofi-Aventis. Archived ...
Amodiaquine Artemether Artemether/lumefantrine Artesunate Artesunate/amodiaquine Artesunate/mefloquine Chloroquine Doxycycline ... To be used in combination with either amodiaquine, mefloquine or sulfadoxine + pyrimethamine. Other combinations that deliver ...
Artesunate Amodiaquine Winthrop (artesunate, amodiaquine) [summary of product characteristics]. Gentilly, France: Sanofi- ... Therefore, it is theoretically possible that the combination of montelukast with a CYP2C8 substrate (e.g. amodiaquine, an anti- ... Hepatotoxicity due to a drug interaction between amodiaquine plus artesunate and efavirenz. Clin Infect Dis. 2007;44(6):889-891 ...
"Geographic patterns of Plasmodium falciparum drug resistance distinguished by differential responses to amodiaquine and ...
Artesunate combination drugs (such as artesunate/amodiaquine and artesunate/mefloquine) are more effective than artemether- ... "The initial pharmaceutical development of an artesunate/amodiaquine oral formulation for the treatment of malaria: a public- ...
In Bobo-Dioulasso, where primaquine was used in combination with either chloroquine or amodiaquine, the prevalence of ... 1999). "[Assay of sensitivity of Plasmodium falciparum to chloroquine, amodiaquine, piperaquine, mefloquine and quinine in ...
Amodiaquine is a 4-aminoquinolone anti-malarial drug similar in structure and mechanism of action to chloroquine. Amodiaquine ... Amodiaquine is now available in a combined formulation with artesunate (ASAQ) and is among the artemisinin-combination ... According to WHO guidelines 2010, artemisinin-based combination therapies should be used in preference to amodiaquine plus ...
A trial conducted in northern Tanzania using the antimalarial drug amodiaquine instead of S/P was similarly successful. Six ... Effect of intermittent treatment with amodiaquine on anaemia and malarial fevers in infants in Tanzania: a randomised placebo- ... Treating schoolchildren in Kenya with S/P and amodiaquine significantly improved anaemia (RR 0.52, 95% CI 0.29-0.93). IPTp ...
"Argemone mexicana decoction versus artesunate-amodiaquine for the management of malaria in Mali: Policy and public-health ...
Lacaze Catherine (2011). "The initial pharmaceutical development of an artesunate/amodiaquine oral formulation for the ... this antimalarial product is a fixed-dose combination of artesunate/amodiaquine (ASAQ). It is the result of a partnership ...
Amodiaquine, or the Combination in Pregnant Women in Ghana". The Journal of Infectious Diseases. 198 (8): 1202-1211. doi: ...
Active Comparator: co-formulated Amodiaquine-Artesunate Sanofi Coarsucam Infant dose (2-12 months/4.5-8kg), amodiaquine:67.5mg/ ... Drug: amodiaquine-artesunate (AQAS) fixed-dose Drug: Artemether-lumefantrine combination (AL) dispersable Not Applicable ... Amodiaquine. Antimalarials. Antiprotozoal Agents. Antiparasitic Agents. Anti-Infective Agents. Antineoplastic Agents. Antiviral ... Sanofi Coarsucam Young Child (13-59 months/9-17kg), amodiaquine: 136mg/artesunate 50mg; 1 tablet once a day for 3 days. ...
Amodiaquine is a 4-aminoquinoline compound related to chloroquine. Amodiaquine was first made in 1948. It is on the World ... "Amodiaquine". International Drug Price Indicator Guide. Retrieved 4 December 2015. "Amodiaquine". Livertox. Archived from the ... Amodiaquine has become an important drug in the combination therapy for malaria treatment in Africa. It is often used in ... Among amodiaquine users, several rare but serious side effects have been reported and linked to variants in the CYP2C8 alleles ...
Artesunate and amodiaquine are both antimalarial medication; however, work by different mechanisms. Artesunate/amodiaquine was ... "Artesunate + Amodiaquine". International Drug Price Indicator Guide. Retrieved 8 December 2016. "Artesunate Amodiaquine ... Artesunate/amodiaquine, sold under the trade name Camoquin among others, is a medication used for the treatment of malaria. It ... Artesunate/amodiaquine is available as a generic medication. The wholesale cost in the developing world is about 0.85 to 1.52 ...
... Peace Mayen Edwin Ubulom, Chinweizu Ejikeme Udobi, and Mark ...
Therapeutic efficacy of sulfadoxine-pyrimethamine, amodiaquine and the sulfadoxine-pyrimethamine-amodiaquine combination ... Therapeutic efficacy of sulfadoxine-pyrimethamine, amodiaquine and the sulfadoxine-pyrimethamine-amodiaquine combination ... Amodiaquine : a case for reconsideration? : reports on individual drugs. No Electronic Version ... Unknown author (‎1996)‎. Amodiaquine : a case for reconsideration? : reports on individual drugs. http://www.who.int/iris/ ...
Amodiaquine + SP is not well tolerated and a substantial proportion of patients experienced pruritus and fatigue, thus ... Tolerability of amodiaquine and sulphadoxine-pyrimethamine, alone or in combination for the treatment of uncomplicated ... Keywords: Plasmodium falciparum malaria; Rwanda; amodiaquine; sulphadoxine-pyrimethamine; tolerability Document Type: Research ... To assess the tolerability and efficacy of amodiaquine (AQ) + sulphadoxine-pyrimethamine (SP), the first-line malaria treatment ...
... *Download PDF Copy ... This orally available drug combination - nelfinavir -amodiaquine - inhibits the virus infection in cell cultures, Kainov said ... The six drugs were nelfinavir, salinomycin, amodiaquine, obatoclax, emetine and homoharringtonine, said Denis Kainov, an ... A combination of nelfinar and amodiaquine exhibited the highest synergy, he said. ...
Amodiaquine-induced reproductive toxicity in adult male rats.. [Yan-Ru Niu, Bing Wei, Bi Chen, Li-Hua Xu, Xia Jing, Cai-Ling ... Amodiaquine (AQ) is routinely prescribed as an anti-malarial drug. Here, we evaluated AQ-induced toxicity in the male ...
... hepatic microsomes despite extensive turnover of amodiaquine to desethylamodiaquine. 5. Amodiaquine quinoneimine underwent ... Role of hepatic metabolism in the bioactivation and detoxication of amodiaquine.. Jewell H1, Maggs JL, Harrison AC, ONeill PM ... This indicated a role for P450 in the bioactivation of amodiaquine to a reactive metabolite that conjugates with glutathione ... Therefore in vitro studies may underestimate the bioactivation of amodiaquine in vivo. These data indicate that the extent of ...
Home , SPAQ-CO™/Supyra® (sulfadoxine-pyrimethamine + amodiaquine). SPAQ-CO™/Supyra® (sulfadoxine-pyrimethamine + amodiaquine) [ ... In March 2012, WHO recommended SMC using a complete treatment of sulfadoxine-pyrimethamine and amodiaquine (SPAQ) once a month ... Source URL: https://www.mmv.org/access/products-projects/spaq-co-supyra-sulfadoxine-pyrimethamine-amodiaquine ... 1] https://www.mmv.org/access/products-projects/spaq-co-supyra-sulfadoxine-pyrimethamine-amodiaquine. ...
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Amodiaquine (AQ) is paired with artesunate (AS) or sulfadoxine-pyrimethamine (SP) in recommended antimalarial regimens. It is ... Selection of parasites with diminished drug susceptibility by amodiaquine-containing antimalarial regimens in Uganda.. Nawaz F1 ... Selection of Parasites with Diminished Drug Sensitivity by Amodiaquine-Containing Antimalarial Regimens in Uganda ... Selection of Parasites with Diminished Drug Sensitivity by Amodiaquine-Containing Antimalarial Regimens in Uganda ...
Background: Amodiaquine has been widely used to treat malaria. Fatal adverse reactions have been reported in adults taking it ... Amodiaquine was more effective than chloroquine for parasite clearance (day 7, Peto odds ratio 4.42 (95% confidence interval ... Objectives: to compare amodiaquine with chloroquine or sulfadoxine-pyrimethamine for treating uncomplicated Plasmodium ... Authors conclusions: There is evidence to support the continued use of amodiaquine to treat uncomplicated malaria, although ...
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Amodiaquine-lnduced Hepatitis: A Report of Seven Cases DOMINIQUE LARREY, M.D.; ANNE CASTOT, M.D.; DOMINIQUE PESSAYRE, M.D.; ... Amodiaquine-lnduced Hepatitis: A Report of Seven Cases. Ann Intern Med. 1986;104:801-803. doi: 10.7326/0003-4819-104-6-801 ... Seven patients developed hepatitis after receiving amodiaquine for malaria prophylaxis for 4 to 15 weeks. Four patients had a ... which is consistent with an immunoallergic mechanism for amodiaquine-induced hepatitis. ...
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Amodiaquine for treating malaria. *Rectal artesunate for treating people with suspected severe malaria before transfer to ... Sulfadoxine-pyrimethamine plus amodiaquine (SP plus AQ) performed better than sulfadoxine-pyrimethamine plus artesunate (SP ... Chloroquine or amodiaquine combined with sulfadoxine-pyrimethamine for treating uncomplicated malaria. *Artesunate plus ... To compare sulfadoxine-pyrimethamine plus amodiaquine (SP plus AQ) with sulfadoxine-pyrimethamine plus artesunate (SP plus AS) ...
... where resistance to amodiaquine is low, the combination of artesunate plus amodiaquine may delay or prevent the emergence of ... plus amodiaquine (a long half-life drug that is presently used in loose combination in many countries). The short half-life ... of a fixed combination of artesunate plus amodiaquine by the Drugs for Neglected Diseases initiative with sanofi-aventis as the ...
... effects of ACT partner drugs have been reported but with little information regarding widely used artesunate/amodiaquine (ASAQ ... resistance-associated genotypes and major increases in genotypes associated with high sensitivity/efficacy for amodiaquine than ... Increased Sensitivity of Plasmodium falciparum to Artesunate/Amodiaquine Despite 14 Years as First-Line Malaria Treatment, ... Increased Sensitivity of Plasmodium falciparum to Artesunate/Amodiaquine Despite 14 Years as First-Line Malaria Treatment, ...
ATAQ EASY: Artesunate + Amodiaquine Fixed Dose Combination in the Treatment of Uncomplicated Plasmodium Falciparum Malaria. The ... history of hepatic and (or) haematological impairment during treatment with amodiaquine. *intake of medication metabolised by ... patient having received artesunate + amodiaquine or artemether + lumefantrine at a suitable dosage within 30 days prior to ... Amodiaquine Fixed-Dose Combination) Administered in 1 or 2 Intakes Per Day Versus Coartem® (Artemether + Lumefantrine) in the ...
... effects of ACT partner drugs have been reported but with little information regarding widely used artesunate/amodiaquine (ASAQ ... resistance-associated genotypes and major increases in genotypes associated with high sensitivity/efficacy for amodiaquine than ... Selection of pfmdr1 mutations after amodiaquine monotherapy and amodiaquine plus artemisinin combination therapy in East Africa ... Beer N, Ali AS, Rotllant G, Abass AK, Omari RS, Al-mafazy AWH, et al. Adherence to artesunate-amodiaquine combination therapy ...
T. K. Mutabingwa, D. Anthony, A. Heller et al., "Amodiaquine alone, amodiaquine+sulfadoxine-pyrimethamine, amodiaquine+ ... D. Schellenberg, E. Kahigwa, C. Drakeley et al., "The safety and efficacy of sulfadoxine-pyrimethamine, amodiaquine, and their ... Efficacy of Artesunate + Sulphadoxine-Pyrimethamine (AS + SP) and Amodiaquine + Sulphadoxine-Pyrimethamine (AQ + SP) for ...
  • The ratio of artesunate: amodiaquine in the formulation is not consistent with the recommendation of the WHO Guidelines for the Treatment of Malaria, thus delivering a lower dose of amodiaquine. (who.int)
  • Thus only about 80% of patients are predicted to receive a therapeutic dose of amodiaquine. (who.int)
  • Authors' conclusions: There is evidence to support the continued use of amodiaquine to treat uncomplicated malaria, although local drug resistance patterns need to be considered. (www.gov.uk)
  • In addition, selection of resistance/tolerance to the slowly eliminated long-acting partner drugs in ACT (e.g., amodiaquine) is expected, especially in highly malaria-endemic areas of Africa ( 8 - 10 ), which could result in relatively reduced ACT cure rates and reduced protection against artemisinin resistance ( 11 ). (cdc.gov)
  • In light of reports of increasing resistance of parasites to amodiaquine in African countries in whichPlasmodium falciparumis endemic as well as the paucity of recent in vitro sensitivity data, we assessed the in vivo and in vitro sensitivity to amodiaquine ofP. (ovid.com)
  • The high prevalence of in vitro and in vivo resistance precludes the use of amodiaquine on its own as second-line treatment. (ovid.com)
  • These findings also suggest that the value of amodiaquine combinations as first- or second-line treatment in areas with similar patterns of 4-aminoquinoline resistance should be reassessed. (ovid.com)
  • This study shows that amodiaquine is effective, safe and affordable in an area with high resistance to chloroquine. (msf.org)
  • We provide in vivo data to support the in vitro correlation between pfcrt SVMNT and increased resistance to the metabolite of amodiaquine. (lshtm.ac.uk)
  • To examine the importance of these mutations in amodiaquine-treated Asian parasites, we determined pre- and posttreatment genotypes for amodiaquine treatment failures from a clinical trial in Afghanistan. (lshtm.ac.uk)
  • Therefore in vitro studies may underestimate the bioactivation of amodiaquine in vivo. (nih.gov)
  • In vivo administration of a small dose amodiaquine dramatically enhanced the effect of histamine on the gastric secretion in dogs . (selleckchem.com)
  • We have compared the ex vivo antimalarial activity of 12 new quinoline di-Mannich base compounds containing the 7-dichloroquinoline or 7-trifluoromethylquinoline nucleus with amodiaquine, chloroquine, and pyronaridine using the Saimiri-bioassay model. (asm.org)
  • This indicated a role for P450 in the bioactivation of amodiaquine to a reactive metabolite that conjugates with glutathione and protein. (nih.gov)
  • In contrast to other antimalarial agents, amodiaquine (because it contains a 4-aminophenol function) depleted glutathione in activated neutrophils, by formation of an electrophilic quinoneimine metabolite. (aspetjournals.org)
  • Insertion of an N-hydroxyethyl function enabled partial clearance of amodiaquine and its deshydroxyfluoro analogue via O-glucuronidation and altered the balance between phase I oxidation and direct phase II conjugation of amodiaquine. (nih.gov)
  • Recently a new series of amodiaquine analogs, in which the hydroxyl group at the 4' position was replaced by various amino groups, was designed. (rroij.com)
  • Role of hepatic metabolism in the bioactivation and detoxication of amodiaquine. (nih.gov)
  • However, no such binding was observed with human (six individuals) hepatic microsomes despite extensive turnover of amodiaquine to desethylamodiaquine. (nih.gov)
  • Amodiaquine prevents severe hepatic injury and high lethality in P. acnes-primed and LPS-induced hepatitis mice. (selleckchem.com)
  • Amodiaquine is actually a congener of chloroquine and is no longer used abroad owing to its propensity for causing hepatic damage and agranulocytosis. (brainkart.com)
  • Among amodiaquine users, several rare but serious side effects have been reported and linked to variants in the CYP2C8 alleles. (wikipedia.org)