Quinolines substituted in any position by one or more amino groups.
An aminoquinoline that is given by mouth to produce a radical cure and prevent relapse of vivax and ovale malarias following treatment with a blood schizontocide. It has also been used to prevent transmission of falciparum malaria by those returning to areas where there is a potential for re-introduction of malaria. Adverse effects include anemias and GI disturbances. (From Martindale, The Extra Pharmacopeia, 30th ed, p404)
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.
Substances that are toxic to blood in general, including the clotting mechanism; hematotoxins may refer to the hematopoietic system.
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)
A phospholipid-interacting antimalarial drug (ANTIMALARIALS). It is very effective against PLASMODIUM FALCIPARUM with very few side effects.
A 4-aminoquinoline compound with anti-inflammatory properties.
A disease-producing enzyme deficiency subject to many variants, some of which cause a deficiency of GLUCOSE-6-PHOSPHATE DEHYDROGENASE activity in erythrocytes, leading to hemolytic anemia.
A genus of protozoa that comprise the malaria parasites of mammals. Four species infect humans (although occasional infections with primate malarias may occur). These are PLASMODIUM FALCIPARUM; PLASMODIUM MALARIAE; PLASMODIUM OVALE, and PLASMODIUM VIVAX. Species causing infection in vertebrates other than man include: PLASMODIUM BERGHEI; PLASMODIUM CHABAUDI; P. vinckei, and PLASMODIUM YOELII in rodents; P. brasilianum, PLASMODIUM CYNOMOLGI; and PLASMODIUM KNOWLESI in monkeys; and PLASMODIUM GALLINACEUM in chickens.
A species of protozoa that is the causal agent of falciparum malaria (MALARIA, FALCIPARUM). It is most prevalent in the tropics and subtropics.
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.
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.
Preclinical testing of drugs in experimental animals or in vitro for their biological and toxic effects and potential clinical applications.
A chemotherapeutic agent that acts against erythrocytic forms of malarial parasites. Hydroxychloroquine appears to concentrate in food vacuoles of affected protozoa. It inhibits plasmodial heme polymerase. (From Gilman et al., Goodman and Gilman's The Pharmacological Basis of Therapeutics, 9th ed, p970)
Economic aspects of the nursing profession.
Drugs that are used to treat RHEUMATOID ARTHRITIS.
A drug that is used in the management of inflammatory bowel diseases. Its activity is generally considered to lie in its metabolic breakdown product, 5-aminosalicylic acid (see MESALAMINE) released in the colon. (From Martindale, The Extra Pharmacopoeia, 30th ed, p907)
The processes of milk secretion by the maternal MAMMARY GLANDS after PARTURITION. The proliferation of the mammary glandular tissue, milk synthesis, and milk expulsion or let down are regulated by the interactions of several hormones including ESTRADIOL; PROGESTERONE; PROLACTIN; and OXYTOCIN.
A chronic form of cutaneous lupus erythematosus (LUPUS ERYTHEMATOSUS, CUTANEOUS) in which the skin lesions mimic those of the systemic form but in which systemic signs are rare. It is characterized by the presence of discoid skin plaques showing varying degrees of edema, erythema, scaliness, follicular plugging, and skin atrophy. Lesions are surrounded by an elevated erythematous border. The condition typically involves the face and scalp, but widespread dissemination may occur.
A procedure consisting of a sequence of algebraic formulas and/or logical steps to calculate or determine a given task.

Central nervous system-mediated hyperglycemic effects of NIK-247, a cholinesterase inhibitor, and MKC-231, a choline uptake enhancer, in rats. (1/943)

We investigated the effects of intracerebroventricular administration of NIK-247 (9-amino-2,3,5,6,7,8-hexahydro-1H-cyclo-penta(b)-quinoline monohydrate hydrochloride; a cholinesterase inhibitor) or MKC-231 (2-(2-oxypyrrolidin-1-yl)-N-(2,3-dimethyl-5,6,7,8-tetrahydrofur o[2,3-b]quinolin-4-yl) acetoamide; a choline uptake enhancer) on plasma glucose level in comparison with that of neostigmine administration in rats. The extents of NIK-247- and MKC-231-induced hyperglycemia were considerably less than that by neostigmine, suggesting that the potencies of the drugs to produce the peripheral hyperglycemia may be pharmacologically negligible.  (+info)

The immune response modifier imiquimod requires STAT-1 for induction of interferon, interferon-stimulated genes, and interleukin-6. (2/943)

Imiquimod is an oral inducer of interferon (IFN) and several other proinflammatory cytokines and has been successfully used topically as an antiviral agent for the treatment of genital warts. We have investigated the molecular mechanisms by which imiquimod induces the expression of IFNs, IFN-stimulated genes (ISGs), and proinflammatory cytokines in vivo, using mice deficient in various components of the IFN signaling system. Mice deficient in the transcription factor interferon regulatory factor 1 (IRF-1) or in the serine/threonine protein kinase PKR responded normally to imiquimod, producing high levels of circulating IFN and induction of several ISGs. On the other hand, when mice deficient in STAT-1 were treated, a 32-fold reduction in the level of circulating IFN was observed, together with a lack of induction of 2-5 oligo adenylate synthetase (2-5 OAS) and IRF-1 genes. Interestingly, there was also a lack of induction of interleukin-6 (IL-6) gene expression, although tumor necrosis factor was induced and readily detected in serum. In mice deficient in the type I IFN receptor, imiquimod induced levels of IFN similar to those in control mice, but again, neither 2-5 OAS, IRF-1, nor IL-6 genes were induced in mutant mice. Our results suggest that STAT-1 plays a critical role in the mechanism of gene activation by imiquimod. Moreover, induction of IL-6 gene expression appears to be dependent on components of the IFN signaling cascade.  (+info)

Nitric oxide inhibits L-type Ca2+ current in glomus cells of the rabbit carotid body via a cGMP-independent mechanism. (3/943)

Previous studies have shown that nitric oxide (NO) inhibits carotid body sensory activity. To begin to understand the cellular mechanisms associated with the actions of NO in the carotid body, we monitored the effects of NO donors on the macroscopic Ca2+ current in glomus cells isolated from rabbit carotid bodies. Experiments were performed on freshly dissociated glomus cells from adult rabbit carotid bodies using the whole cell configuration of the patch-clamp technique. The NO donors sodium nitroprusside (SNP; 600 microM, n = 7) and spermine nitric oxide (SNO; 100 microM, n = 7) inhibited the Ca2+ current in glomus cells in a voltage-independent manner. These effects of NO donors were rapid in onset and peaked within 1 or 2 min. In contrast, the outward K+ current was unaffected by SNP (600 microM, n = 6), indicating that the inhibition by SNP was not a nonspecific membrane effect. 2-(4-carboxyphenyl)-4,4,5, 5-tetramethyl-imidazoline-1-oxyl-3-oxide (carboxy-PTIO; 500 microM), an NO scavenger, prevented inhibition of the Ca2+ current by SNP (n = 7), whereas neither superoxide dismutase (SOD; 2,000 U/ml, n = 4), a superoxide scavenger, nor sodium hydrosulfite (SHS; 1 mM, n = 7), a reducing agent, prevented inhibition of the Ca2+ current by SNP. However, SNP inhibition of the Ca2+ current was reversible in the presence of either SOD or SHS. These results suggest that NO itself inhibits Ca2+ current in a reversible manner and that subsequent formation of peroxynitrites results in irreversible inhibition. SNP inhibition of the Ca2+ current was not affected by 30 microM LY 83, 583 (n = 7) nor was it mimicked by 600 microM 8-bromoguanosine 3':5'-cyclic monophosphate (8-Br-cGMP; n = 6), suggesting that the effects of NO on the Ca2+ current are mediated, in part, via a cGMP-independent mechanism. N-ethylmaleimide (NEM; 2.5 mM, n = 6) prevented the inhibition of the Ca2+ current by SNP, indicating that SNP is acting via a modification of sulfhydryl groups on Ca2+ channel proteins. Norepinephrine (NE; 10 microM) further inhibited the Ca2+ current in the presence of NEM (n = 7), implying that NEM did not nonspecifically eliminate Ca2+ current modulation. Nisoldipine, an L-type Ca2+ channel blocker (2 microM, n = 6), prevented the inhibition of Ca2+ current by SNP, whereas omega-conotoxin GVIA, an N-type Ca2+ channel blocker (1 microM, n = 9), did not prevent the inhibition of Ca2+ current by SNP. These results demonstrate that NO inhibits L-type Ca2+ channels in adult rabbit glomus cells, in part, due to a modification of calcium channel proteins. The inhibition might provide one plausible mechanism for efferent inhibition of carotid body activity by NO.  (+info)

Possible novel mechanism for bitter taste mediated through cGMP. (4/943)

Taste is the least understood among sensory systems, and bitter taste mechanisms pose a special challenge because they are elicited by a large variety of compounds. We studied bitter taste signal transduction with the quench-flow method and monitored the rapid kinetics of the second messenger guanosine 3',5'-cyclic monophosphate (cGMP) production and degradation in mouse taste tissue. In response to the bitter stimulants, caffeine and theophylline but not strychnine or denatonium cGMP levels demonstrated a rapid and transient increase that peaked at 50 ms and gradually declined throughout the following 4.5 s. The theophylline- and caffeine-induced effect was rapid, transient, concentration dependent and gustatory tissue-specific. The effect could be partially suppressed in the presence of the soluble guanylyl cyclase (GC) inhibitor 10 microM ODQ and 30 microM methylene blue but not 50 microM LY 83583 and boosted by nitric oxide donors 25 microM NOR-3 or 100 microM sodium nitroprusside. The proposed mechanism for this novel cGMP-mediated bitter taste signal transduction is cGMP production partially by the soluble GC and caffeine-induced inhibition of one or several phosphodiesterases.  (+info)

Treatment of experimental leishmaniasis with the immunomodulators imiquimod and S-28463: efficacy and mode of action. (5/943)

There is a need for new, effective, and less toxic treatments for leishmaniasis, an infectious disease caused by Leishmania protozoa and is a major cause of suffering and morbidity in much of the developing world. Imiquimod, an immune-response modifier, has recently been approved by the Food and Drug Administration for the treatment of genital warts caused by human papillomaviruses. Imiquimod initiates a local immune reaction, including the stimulation of macrophages, resulting in resolution of human papillomavirus infection and regression of the viral lesion. Since imiquimod activates a number of immune cells, including macrophages, which are the only host cells of Leishmania species, an investigation was done to determine whether it induces leishmanicidal properties in infected macrophages in vitro and in vivo in a mouse model. Imiquimod and a related compound, S-28463, effectively stimulated leishmanicidal activity in macrophages; moreover, imiquimod stimulated signal transduction associated with inducing nitric oxide synthesis in macrophages.  (+info)

Protection against hydrogen peroxide cytotoxicity in rat-1 fibroblasts provided by the oncoprotein Bcl-2: maintenance of calcium homoeostasis is secondary to the effect of Bcl-2 on cellular glutathione. (6/943)

The oncoprotein Bcl-2 protects cells against apoptosis, but the exact molecular mechanism that underlies this function has not yet been identified. Studying H2O2-induced cell injury in Rat-1 fibroblast cells, we observed that Bcl-2 had a protective effect against the increase in cytosolic calcium concentration and subsequent cell death. Furthermore, overexpression of Bcl-2 resulted in an alteration of cellular glutathione status: the total amount of cellular glutathione was increased by about 60% and the redox potential of the cellular glutathione pool was maintained in a more reduced state during H2O2 exposure compared with non-Bcl-2-expressing controls. In our cytotoxicity model, disruption of cellular glutathione homoeostasis closely correlated with the pathological elevation of cytosolic calcium concentration. Stabilization of the glutathione pool by Bcl-2, N-acetylcysteine or glucose delayed the cytosolic calcium increase and subsequent cell death, whereas depletion of glutathione by dl-buthionine-(S, R)-sulphoximine, sensitized Bcl-2-transfected cells towards cytosolic calcium increase and cell death. We therefore suggest that the protection exerted by Bcl-2 against H2O2-induced cytosolic calcium elevation and subsequent cell death is secondary to its effect on the cellular glutathione metabolism.  (+info)

Nitric oxide stimulates cGMP production and mimics synaptic responses in metacerebral neurons of Aplysia. (7/943)

Nitric oxide (NO) acts as a neurotransmitter and neuromodulator in the nervous systems of many vertebrates and invertebrates. We investigated the mechanism of NO action at an identified synapse between a mechanoafferent neuron, C2, and the serotonergic metacerebral cell (MCC) in the cerebral ganglion of the mollusc Aplysia californica. Stimulation of C2 produces a decreasing conductance, very slow EPSP in the MCC. C2 is thought to use histamine and NO as cotransmitters at this synapse, because both agents mimic the membrane responses. Now we provide evidence that treatment with NO donors stimulates soluble guanylyl cyclase (sGC) in the MCC, and as a result cGMP increases. S-Nitrosocysteine (SNC, an NO donor) and 8-bromo-cGMP (8-Br-cGMP) both induced the membrane depolarization and increase in input resistance that are characteristic of the very slow EPSP. Two inhibitors of sGC, 6-anilino-5,8-quinolinequinone (LY83583) and 1H-[1,2,4]oxadiazolo[4, 3-a]quinoxaline-1-one (ODQ), suppressed both the very slow EPSP and the membrane responses to SNC but not the histamine membrane responses. NO-induced cGMP production was determined in the MCC using cGMP immunocytochemistry (cGMP-IR). In the presence of 3-isobutyl-1-methylxanthine (IBMX), 10 microM SNC was sufficient to induce cGMP-IR, and the staining intensity increased as the SNC dose was increased. This cGMP-IR was suppressed by ODQ in a dose-dependent manner and completely blocked by 10 microM ODQ. Histamine did not induce cGMP-IR. The results suggest that NO stimulates sGC-dependent cGMP synthesis in the MCC and that cGMP mediates the membrane responses. The cotransmitter histamine induces essentially the same membrane responses but seems to use a separate and distinct second messenger pathway.  (+info)

Histochemically reactive zinc in plaques of the Swedish mutant beta-amyloid precursor protein transgenic mice. (8/943)

Endogenous metals such as zinc may contribute to beta-amyloid (Abeta) aggregation and hence the plaque formation. In the present study, we examined brains of four Swedish mutant amyloid precursor protein (APP) transgenic mice at 12 months of age for histochemically reactive zinc in the plaques. Here, we report that all the Congo red (+) mature plaques contained chelatable zinc, as demonstrated by staining with the zinc-specific fluorescent dye 6-methoxy-8-quinolyl-para-toluenesulfonamide (TSQ). On the other hand, Congo red (-) preamyloid Abeta deposits were not stained with TSQ. Interestingly, although cerebellum contained similar degree of preamyloid Abeta deposits as cerebral cortex, it was completely devoid of Congo red- or TSQ-stained mature plaques. Although zinc from plaques was only slowly and partially removed by a specific zinc remover, dithizone, treatment of brain sections with heparinase-III, which degrades heparan sulfate proteoglycan (HSPG), another major constituent of plaques, greatly fastened the zinc removal with dithizone. The present study has demonstrated the presence of histochemically reactive zinc in plaques, but not preamyloid Abeta deposits, of the Swedish mutant APP transgenic mice. Because preamyloid Abeta deposits fail to develop into congophilic plaques in cerebellum where synaptic vesicle zinc is deficient, the synaptic zinc may be a necessary element in the plaque formation. In holding zinc inside plaques, HSPG may contribute in addition to Abeta.  (+info)

The condition is inherited in an X-linked recessive pattern, meaning that the gene for G6PD deficiency is located on the X chromosome and affects males more frequently than females. Females may also be affected but typically have milder symptoms or may be carriers of the condition without experiencing any symptoms themselves.

G6PD deficiency can be caused by mutations in the G6PD gene, which can lead to a reduction in the amount of functional enzyme produced. The severity of the condition depends on the specific nature of the mutation and the degree to which it reduces the activity of the enzyme.

Symptoms of G6PD deficiency may include jaundice (yellowing of the skin and eyes), fatigue, weakness, and shortness of breath. In severe cases, the condition can lead to hemolytic anemia, which is characterized by the premature destruction of red blood cells. This can be triggered by certain drugs, infections, or foods that contain high levels of oxalic acid or other oxidizing agents.

Diagnosis of G6PD deficiency typically involves a combination of clinical evaluation, laboratory tests, and genetic analysis. Treatment is focused on managing symptoms and preventing complications through dietary modifications, medications, and avoidance of triggers such as certain drugs or infections.

Overall, G6PD deficiency is a relatively common genetic disorder that can have significant health implications if left untreated. Understanding the causes, symptoms, and treatment options for this condition is important for ensuring appropriate care and management for individuals affected by it.

There are several different types of malaria, including:

1. Plasmodium falciparum: This is the most severe form of malaria, and it can be fatal if left untreated. It is found in many parts of the world, including Africa, Asia, and Latin America.
2. Plasmodium vivax: This type of malaria is less severe than P. falciparum, but it can still cause serious complications if left untreated. It is found in many parts of the world, including Africa, Asia, and Latin America.
3. Plasmodium ovale: This type of malaria is similar to P. vivax, but it can cause more severe symptoms in some people. It is found primarily in West Africa.
4. Plasmodium malariae: This type of malaria is less common than the other three types, and it tends to cause milder symptoms. It is found primarily in parts of Africa and Asia.

The symptoms of malaria can vary depending on the type of parasite that is causing the infection, but they typically include:

1. Fever
2. Chills
3. Headache
4. Muscle and joint pain
5. Fatigue
6. Nausea and vomiting
7. Diarrhea
8. Anemia (low red blood cell count)

If malaria is not treated promptly, it can lead to more severe complications, such as:

1. Seizures
2. Coma
3. Respiratory failure
4. Kidney failure
5. Liver failure
6. Anemia (low red blood cell count)

Malaria is typically diagnosed through a combination of physical examination, medical history, and laboratory tests, such as blood smears or polymerase chain reaction (PCR) tests. Treatment for malaria typically involves the use of antimalarial drugs, such as chloroquine or artemisinin-based combination therapies. In severe cases, hospitalization may be necessary to manage complications and provide supportive care.

Prevention is an important aspect of managing malaria, and this can include:

1. Using insecticide-treated bed nets
2. Wearing protective clothing and applying insect repellent when outdoors
3. Eliminating standing water around homes and communities to reduce the number of mosquito breeding sites
4. Using indoor residual spraying (IRS) or insecticide-treated wall lining to kill mosquitoes
5. Implementing malaria control measures in areas where malaria is common, such as distribution of long-lasting insecticidal nets (LLINs) and indoor residual spraying (IRS)
6. Improving access to healthcare services, particularly in rural and remote areas
7. Providing education and awareness about malaria prevention and control
8. Encouraging the use of preventive medications, such as intermittent preventive treatment (IPT) for pregnant women and children under the age of five.

Early diagnosis and prompt treatment are critical in preventing the progression of malaria and reducing the risk of complications and death. In areas where malaria is common, it is essential to have access to reliable diagnostic tools and effective antimalarial drugs.

It is important for individuals with discoid lupus erythematosus to be aware of their condition and seek medical attention if they experience any changes in their symptoms or if new lesions develop, as the disease can lead to complications such as skin cancer, scarring, and joint pain if left untreated. Early diagnosis and treatment can help prevent these complications and improve quality of life for those affected by the condition.

Depending upon the location of the amino group, they can be divided into: 4-Aminoquinoline 8-Aminoquinoline This set index page ... Aminoquinolines are derivatives of quinoline, most notable for their roles as antimalarial drugs. ...
... is a form of aminoquinoline with the amino group at the 4-position of the quinoline. The compound has been ... "4-Aminoquinoline 578-68-7 , TCI America". www.tcichemicals.com. Retrieved 2020-03-06. v t e (Articles without InChI source, ... Bourne SA, De Villiers K, Egan TJ (2006). "Three 4-aminoquinolines of antimalarial interest". Acta Crystallogr C. 62 (Pt 2): ... Bray PG, Hawley SR, Ward SA (1996). "4-Aminoquinoline resistance of Plasmodium falciparum: insights from the study of ...
... is the 8-amino derivative of quinoline. Often abbreviated AQ, it is a pale yellow solid. It is structurally ... 1997). "X-ray and vibrational studies of 8-aminoquinoline. Evidence for a three-center hydrogen bond". Journal of Physical ... Sweeney AW; Blackburn CRB; KH Rieckmann (1 August 2004). "Short report: The activity of pamaquine, an 8-aminoquinoline drug, ... Corbet, Matthieu; De Campo, Floryan (2013). "8-Aminoquinoline: A Powerful Directing Group in Metal-Catalyzed Direct ...
... and clearance of liver forms with an 8-aminoquinoline agent such as primaquine or tafenoquine. The view that 8-aminoquinoline ... Waters NC, Edstein MD (2012). "8-Aminoquinolines: Primaquine and tafenoquine". In Staines HM, Krishna S (eds.). Treatment and ... Cochrane Infectious Diseases Group) (February 2018). "Primaquine or other 8-aminoquinolines for reducing Plasmodium falciparum ...
J-113,397 LY-2940094 SB-612,111 Shinkai H, Ito T, Iida T, Kitao Y, Yamada H, Uchida I (November 2000). "4-Aminoquinolines: ...
... is a two-ring heterocyclic compound used as a chemical intermediate to aminoquinoline antimalarial drugs ... US patent 2546658, Surrey, Alexander R, "7-chloro-4-[5-(N-ethyl-N-2-hydroxyethylamino)-2-pentyl] aminoquinoline, its acid ... Raj, Raghu; Land, Kirkwood M.; Kumar, Vipan (2015). "4-Aminoquinoline-hybridization en route towards the development of ... The availability of 4,7-dichloroquinoline allowed alternative structural analogs of the 4-aminoquinoline type to be ...
... is in the 8-aminoquinoline family of medications. How it works is unclear but it is effective both in the liver and ...
... is a 4-aminoquinoline compound related to chloroquine. Amodiaquine was first made in 1948. It is on the World ...
... is a member of the drug class 4-aminoquinoline. As an antimalarial, it works against the asexual form of the ...
US patent 2546658, Surrey, Alexander R, "7-chloro-4-[5-(N-ethyl-N-2-hydroxyethylamino)-2-pentyl] aminoquinoline, its acid ... Hydroxychloroquine is in the antimalarial and 4-aminoquinoline families of medication. Hydroxychloroquine was approved for ... label advises that hydroxychloroquine should not be prescribed to individuals with known hypersensitivity to 4-aminoquinoline ...
Lee, S. J.; Makaravage, K. J.; Brooks, A. F.; Scott, P. J. H.; Sanford, M. S. "Cu‐Mediated Aminoquinoline‐Directed ... "Copper-Mediated Aminoquinoline-Directed Radiofluorination of Aromatic C−H Bonds with K18F". Angewandte Chemie International ...
"Copper-Mediated Aminoquinoline-Directed Radiofluorination of Aromatic C−H Bonds with K18F". Angewandte Chemie International ...
"Formation of derivatives of dioxindole from esters of mesoxalic acid and aromatic amines or amino quinolines". Compt. Rend. 156 ...
... is an 8-aminoquinoline drug formerly used for the treatment of malaria. It is closely related to primaquine. ... Sweeney AW, Blackburn CR, Rieckmann KH (August 2004). "Short report: the activity of pamaquine, an 8-aminoquinoline drug, ...
Bogert, M. T.; Fisher, H. L. (1912). "The Preparation and Properties of 5-Aminoquinoline-6-Carboxylic Acid and Certain Related ... His PhD dissertation focused on the preparation and properties of 5-aminoquinoline-6-carboxylic acid and related compounds. ...
... is an analog of pamaquine which was the first drug of the 8-aminoquinoline class; tafenoquine is another such drug. ...
Two doses of the 8-aminoquinoline plasmoquine were given weekly to workers and their families in two camps. The prevalences of ... For example, the widespread use of 8-aminoquinolines in areas where Glucose-6-phosphate dehydrogenase deficiency is common ...
Most were 8-aminoquinoline compounds, analogs of pamaquine, an existing alternative to quinine that was unfavorable due to its ... primarily from the 8-aminoquinoline group of compounds. The study marked the first human test of the antimalarial drug ...
Resochin (7-chloro-4- 4- (diethylamino) - 1 - methylbutyl amino quinoline) and a similar compound Sontochin (3-methyl Resochin ...
The authors rely on an 8-aminoquinoline directing group to control the regioselectivity of migratory insertion and stabilize ...
... the first synthetic antimalarial compound-Atabrin and this was followed by Resochin and Sontochin derived from 4-aminoquinoline ...
In 2014, Chatani and coworkers proposed that a NiIV intermediate was formed during an aminoquinoline-directed aliphatic C-H ...
... aminoquinolines MeSH D03.438.810.050.060 - amodiaquine MeSH D03.438.810.050.180 - chloroquine MeSH D03.438.810.050.180.350 - ...
Chen and coworkers demonstrated another stereoselective approach, which coupled iodotryptophan to 8-aminoquinoline by palladium ...
It is an 8-aminoquinoline, of the same family as primaquine, developed by researchers at the Walter Reed Army Institute of ...
... alkaloids 4-Aminoquinoline 8-Hydroxyquinoline Pyrroloquinoline quinone (PQQ), a redox cofactor and controversial ...
... a score that measures the ability of a person to deal with adversities in his or her life 8-Aminoquinoline, a heterocyclic ...
The molecular formula C9H8N2 (molar mass: 144.17 g/mol, exact mass: 144.0687 u) may refer to: 4-Aminoquinoline 8-Aminoquinoline ...
2014)‎. Safety of 8-aminoquinoline antimalarial medicines. World Health Organization. https://extranet.who.int/iris/restricted/ ...
Herein, a series of 27 ,i,N,/i,-(4-(benzyloxy)benzyl)-4-aminoquinolines were synthesized and evaluated for their ability to ... Synthesis and Antimycobacterial Evaluation of N-(4-(Benzyloxy)benzyl)-4-aminoquinolines Estevão Silveira Grams 1 2 , Alessandro ... Synthesis and Antimycobacterial Evaluation of N-(4-(Benzyloxy)benzyl)-4-aminoquinolines Estevão Silveira Grams et al. Molecules ... Herein, a series of 27 N-(4-(benzyloxy)benzyl)-4-aminoquinolines were synthesized and evaluated for their ability to inhibit ...
... and bioisosteric ferrocenyl-derived aminoquinoline-benzimidazole hybrid compounds were synthesised and evaluated for their in ... Bioisosteric ferrocenyl aminoquinoline-benzimidazole hybrids: Antimicrobial evaluation and mechanistic insights N Baartzes 1 , ... Bioisosteric ferrocenyl aminoquinoline-benzimidazole hybrids: Antimicrobial evaluation and mechanistic insights N Baartzes et ... Synthesis and in vitro antiplasmodial activity of ferrocenyl aminoquinoline derivatives. Mwande Maguene G, Lekana-Douki JB, ...
Methaemoglobinaemia and the radical curative efficacy of 8‐aminoquinoline antimalarials Share Share Share ...
Nickel-Catalyzed Remote C4-H Arylation of 8-Aminoquinolines. Zhu, Longzhi; Sheng, Xinghao; Li, You; Lu, Dong; Qiu, Renhua; ... A useful and convenient method for C-H bond arylation of 8-aminoquinoline motifs on the remote C4 position was developed. This ... Nickel-Catalyzed Remote C4-H Arylation of 8-Aminoquinolines. ... tolerance toward various Grignard reagents and aminoquinoline ...
Order Aminoquinoline from our webshop * Quinoline in our webshop * Hydroxyquinoline in our webshop ...
8-Aminoquinoline and Malaria have in common. Hyperleap helps uncover and suggest relationships using custom algorithms. ... Primaquine is an analog of pamaquine which was the first drug of the 8-aminoquinoline class; tafenoquine is another such drug. ... and clearance of liver forms with an 8-aminoquinoline agent such as primaquine or tafenoquine. ...
HomeWhats with aminoquinoline directing groups all of a sudden? Whats with aminoquinoline directing groups all of a sudden?. ... all involving various uses of the aminoquinoline amide as a directing group. The number of papers to come out in the past month ...
For radical cure of P. vivax and P. ovale infections, concomitant therapy with an 8-aminoquinoline compound is necessary (see ... The 4-aminoquinoline compounds are very rapidly and completely absorbed after ingestion, and in accidental overdosage, or ... Children are especially sensitive to the 4-aminoquinoline compounds. Most reported fatalities followed the accidental ingestion ... Use of hydroxychloroquine sulfate is contraindicated in patients with known hypersensitivity to 4-aminoquinoline compounds. ...
Other names: Quinoline, 6-amino-; 6-Aminoquinoline; Quinolin-6-ylamine; quinolin-6-amine ...
8-Aminoquinoline Therapy for Latent Malaria. Baird JK. Baird JK. Clin Microbiol Rev. 2019 Jul 31;32(4):e00011-19. doi: 10.1128/ ... Evolution of the 8-aminoquinoline hypnozoitocides, including the winnowing out of irreversible severe neurotoxicity of ... Evolution of the 8-aminoquinoline hypnozoitocides, including the winnowing out of irreversible severe neurotoxicity… ... the US Food and Drug Administration approved the uses of a new hepatic schizontocidal and hypnozoitocidal 8-aminoquinoline ...
Aminoquinolines / therapeutic use Actions. * Search in PubMed * Search in MeSH * Add to Search ...
Categories: Aminoquinolines Image Types: Photo, Illustrations, Video, Color, Black&White, PublicDomain, CopyrightRestricted 1 ...
MeSH Terms: Aminoquinolines; Aniline Compounds; Animals; Aortic Valve/drug effects; Aortic Valve/pathology; Apoptosis/drug ...
Known hypersensitivity to 4-aminoquinoline compounds. *G6PD deficiency. *History of retinopathy. *Have an active infection at ...
8-Aminoquinoline therapy for latent malaria. Clin Microbiol Rev 32: e00011-e00019. ... 8-Aminoquinoline therapy for latent malaria. . Clin Microbiol Rev 32. : e00011. -. e00019. .. ), false ...
For radical cure of P. vivax and P. ovale infections, concomitant therapy with an 8-aminoquinoline drug is necessary [see ... For radical cure of P. vivax and P. ovale infections, concomitant therapy with an 8-aminoquinoline drug is necessary. ... The following adverse reactions have been identified during post-approval use of 4 aminoquinoline drugs, including ... Hydroxychloroquine is a 4-aminoquinoline antimalarial [see Microbiology (12.4)] and antirheumatic agent. ...
Relapse of porphyria cutanea tarda after treatment with phlebotomy or 4-aminoquinoline antimalarials: a meta-analysis. Br J ...
42] However, a report by Salameh indicated that relapses are more common after 4-aminoquinoline treatment as compared with ... Relapse of porphyria cutanea tarda after treatment with phlebotomy or 4-aminoquinoline antimalarials: a meta-analysis. Br J ... Relapse of porphyria cutanea tarda after treatment with phlebotomy or 4-aminoquinoline antimalarials: a meta-analysis. Br J ... Chloroquine and hydroxychloroquine, two antimalarial medications that belong to the 4-aminoquinolines, chelate and remove ...
Hypersensitivity to 4-aminoquinoline derivatives. Cautions. Not effective against chloroquine-resistant strains of P falciparum ... For radical cure of P vivax and P ovale infections, concomitant therapy with an 8-aminoquinoline compound is necessary ... For radical cure of P vivax and P ovale infections, concomitant therapy with an 8-aminoquinoline compound is necessary ... is excreted in human milk and it is known that infants are extremely sensitive to the toxic effects of 4-aminoquinolines ...
Carvalho, L.; Luque-Ortega, J.R.; López-Martín, C.; Castanys, S.; Rivas, L.; Gamarro, F. The 8-aminoquinoline analogue ... an antiplasmodial 8-aminoquinoline, targets Leishmania respiratory complex III and induces apoptosis. Antimicrob. Agents ...
Chemistry: Isolation and Identification of a Pneumocystis carinii protein with affinity for 8-Aminoquinolines ...
Aminoquinolines Preferred Term Term UI T001905. Date01/01/1999. LexicalTag NON. ThesaurusID NLM (1975). ... Aminoquinolines Preferred Concept UI. M0000967. Registry Number. 0. Scope Note. Quinolines substituted in any position by one ... Aminoquinolines. Tree Number(s). D03.633.100.810.050. Unique ID. D000634. RDF Unique Identifier. http://id.nlm.nih.gov/mesh/ ...
  • Among those with G6PD deficiency, hemolytic anemia may be triggered by bacterial or viral infections and by certain foods and drugs, including the 8-aminoquinoline (8-AQ) class of antimalarials. (health.mil)
  • What do Tafenoquine, 8-Aminoquinoline and Malaria have. (hyperleap.com)
  • Tafenoquine is in the 8-aminoquinoline family of medications. (hyperleap.com)
  • In 2018, the US Food and Drug Administration approved the uses of a new hepatic schizontocidal and hypnozoitocidal 8-aminoquinoline called tafenoquine for the respective prevention of all malarias and for the treatment of those that relapse (P. vivax and Plasmodium ovale). (nih.gov)
  • Tafenoquine, an 8-aminoquinoline antimalarial, is active against all the stages of Plasmodium species that include the hypnozoite (dormant stage) in the liver. (drugcentral.org)
  • Providing radical cure for women with 8-aminoquinolines (e.g., primaquine) is hindered by gender-specific complexities. (tropmedres.ac)
  • Chloroquine and hydroxychloroquine, two antimalarial medications that belong to the 4-aminoquinolines, chelate and remove hepatic-bound porphyrins by forming water-soluble complexes that are eliminated in the urine. (medscape.com)
  • Trials of the use of the 4-aminoquinolines, chloroquine and hydroxychloroquine, in the treatment of people with COVID-19, exemplify the problem. (cebm.net)
  • For radical cure of P. vivax and P. ovale infections, concomitant therapy with an 8-aminoquinoline drug is necessary. (nih.gov)
  • Radical cure with an 8-aminoquinoline will be needed for the rapid elimination of vivax malaria. (ox.ac.uk)
  • [ 42 ] However, a report by Salameh indicated that relapses are more common after 4-aminoquinoline treatment as compared with phlebotomy for PCT. (medscape.com)
  • 1,2 For example, members of the 8-aminoquinoline (8-AQ) class of antimalarial drugs can cause hemolysis in the G6PD deficient population. (health.mil)
  • 2014)‎. Safety of 8-aminoquinoline antimalarial medicines. (who.int)