Aminoquinolines: Quinolines substituted in any position by one or more amino groups.Primaquine: 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)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.Hemolytic Agents: Substances that are toxic to blood in general, including the clotting mechanism; hematotoxins may refer to the hematopoietic system.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)Mefloquine: A phospholipid-interacting antimalarial drug (ANTIMALARIALS). It is very effective against PLASMODIUM FALCIPARUM with very few side effects.Amodiaquine: A 4-aminoquinoline compound with anti-inflammatory properties.Glucosephosphate Dehydrogenase Deficiency: 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.Plasmodium: 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.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.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.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.Drug Evaluation, Preclinical: Preclinical testing of drugs in experimental animals or in vitro for their biological and toxic effects and potential clinical applications.

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)

*Aminoquinoline

Depending upon the location of the amino group, they can be divided into: 4-Aminoquinoline 8-Aminoquinoline. ... Aminoquinolines are derivatives of quinoline, most notable for their roles as antimalarial drugs. ...

*4-Aminoquinoline

... is a form of aminoquinoline with the amino group at the 4-position of the quinoline. A variety of derivatives ... Bourne SA, De Villiers K, Egan TJ (2006). "Three 4-aminoquinolines of antimalarial interest". Acta Crystallogr C. 62 (Pt 2): ... Amodiaquine Chloroquine Hydroxychloroquine Bray PG, Hawley SR, Ward SA (1996). "4-Aminoquinoline resistance of Plasmodium ... of 4-aminoquinoline are antimalarial agents useful in treating erythrocytic plasmodial infections. Examples include amodiaquine ...

*8-Aminoquinoline

... is a form of aminoquinoline with an amine at the 8-position of quinoline. The 8-aminoquinoline family of drugs ... The 8-aminoquinoline drugs must not be given to patients with G6PD deficiency, because they cause potentially fatal haemolysis ... an 8-aminoquinoline drug, against sporozoite-induced infections of Plasmodium vivax (New Guinea strains)". Am J Trop Med Hyg. ...

*JTC-801

J-113,397 LY-2940094 SB-612,111 Shinkai H, Ito T, Iida T, Kitao Y, Yamada H, Uchida I (2000). "4-Aminoquinolines: novel ...

*Neocuproine

... and aminoquinoline structures!) (Error! the last step must involve As2O5, not As2O3 as an oxidant in Skraup reaction!): An ...

*Amodiaquine

... is a 4-aminoquinoline compound related to chloroquine. Amodiaquine was first made in 1948. It is on the World ...

*Chloroquine

... is a member of the drug class 4-aminoquinoline. It works against the asexual form of malaria inside the red blood ...

*Pamaquine

... is an 8-aminoquinoline drug used for the treatment of malaria. It is closely related to primaquine. Pamaquine was the ... 1 August 2004). "Short report: The activity of pamaquine, an 8-aminoquinoline drug, against sporozoite-induced infections of ...

*Martinet dioxindole synthesis

"Formation of derivatives of dioxindole from esters of mesoxalic acid and aromatic amines or amino quinolines". Compt. Rend. 156 ...

*Primaquine

... is an analog of pamaquine which was the first drug of the 8-aminoquinoline class; tafenoquine is another such drug. ...

*Mass drug administration

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 ...

*Harry L. Fisher

His PhD dissertation focused on the preparation and properties of 5-aminoquinoline-6-carboxylic acid and related compounds. ...

*Stateville Penitentiary Malaria Study

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 ...

*Amoebic liver abscess

Later when synthetic derivatives of quinine were introduced, chloroquine phosphate, a 4-aminoquinoline was found to be less ...

*Tafenoquine

... is an 8-aminoquinoline drug manufactured by GlaxoSmithKline that is being investigated as a potential treatment for ...

*Malaria prophylaxis

... the first synthetic antimalarial compound-Atabrin and this was followed by Resochin and Sontochin derived from 4-aminoquinoline ...

*List of MeSH codes (D03)

... aminoquinolines MeSH D03.438.810.050.060 --- amodiaquine MeSH D03.438.810.050.180 --- chloroquine MeSH D03.438.810.050.180.350 ...

*Moroidin

Chen and coworkers demonstrated another stereoselective approach, which coupled iodotryptophan to 8-aminoquinoline by palladium ...
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Avoid getting Aldara in your eyes, mouth, and nose, or on your lips. Do not place the cream in your rectum, vagina, or urethra. If it does get into any of these areas, rinse with water. Do not use Aldara on sunburned, windburned, dry, chapped, irritated, or broken skin.. Avoid using other medications on the areas you treat with Aldara unless your doctor tells you to.. Avoid exposure to sunlight or tanning beds. Aldara can make you sunburn more easily. Wear protective clothing and use sunscreen (SPF 30 or higher) when you are outdoors.. Avoid having unprotected sex. Imiquimod is not a cure for genital warts, and it will not protect against sexually transmitted diseases such as chlamydia, gonorrhea, herpes, HIV, syphilis, and trichomoniasis. Talk with your doctor about safe ways to prevent transmission during sex.. SIDE EFFECTS. Get emergency medical help if you have any of these signs of an allergic reaction to Aldara: hives; difficulty breathing; swelling of your face, lips, tongue, or throat. ...
Avoid getting Aldara in your eyes, mouth, and nose, or on your lips. Do not place the cream in your rectum, vagina, or urethra. If it does get into any of these areas, rinse with water. Do not use Aldara on sunburned, windburned, dry, chapped, irritated, or broken skin.. Avoid using other medications on the areas you treat with Aldara unless your doctor tells you to.. Avoid exposure to sunlight or tanning beds. Aldara can make you sunburn more easily. Wear protective clothing and use sunscreen (SPF 30 or higher) when you are outdoors.. Avoid having unprotected sex. Imiquimod is not a cure for genital warts, and it will not protect against sexually transmitted diseases such as chlamydia, gonorrhea, herpes, HIV, syphilis, and trichomoniasis. Talk with your doctor about safe ways to prevent transmission during sex. ...
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In most mammals, prolactin (PRL) is essential for maintaining lactation, and yet the short-term suppression of PRL during established lactation by bromocriptine has produced inconsistent effects on milk yield in cows and goats. To assess the effect of the long-term inhibition of PRL release in lactating dairy cows, 5 Holstein cows in early lactation received daily intramuscular injections of 1mg of the PRL-release inhibitor quinagolide for 9 wk. Four control cows received the vehicle (water) only. During the last week of the treatments, one udder half was milked once a day (1×) and the other twice a day (2×). Blood samples were harvested at milking in wk -1, 1, 4, and 8. The daily injections of quinagolide reduced milking-induced PRL release but not the basal PRL concentration. Quinagolide induced a faster decline in milk production, which was about 5.3 kg/d lower in the quinagolide-treated cows during the last 4 wk of treatment. During wk 9, the inhibition of milk production by quinagolide was
OUTLINE: This is a pilot, prospective, multicenter study.. Patients apply topical imiquimod cream to a target vulvar lesion 3 times weekly. Treatment continues for up to 12 weeks in the absence of disease progression or unacceptable toxicity. If the lesion is still present after completion of 12 weeks of imiquimod therapy, the patient undergoes surgical excision of the target lesion (and any other progressive lesions suspicious for evolving adenocarcinoma) at week 16.. Patients undergo punch biopsy and photographic assessment of a target vulvar lesion at baseline and again at 12 weeks.. After completion of imiquimod therapy or after surgical excision, patients are followed at 6 weeks and then every 3 months for at least 2 years. ...
Chemical shielding tensors are calculated for the carbons in a series of 4-aminoquinolines with different substituents at the 7-position. The 11 component is used as a measure of the relative -electron density at each carbon. By comparing the -electron density at each carbon with the log K of binding to heme (Kaschula et al. J. Med. Chem. 2002, 45, 3531), the drug-heme association is found to increase with increasing -electron density at the carbons meta to the substituent and with decreasing -electron density at the carbons ortho and para to the substituent. The greatest change in -electron density is at the ortho carbons, and log K increases with a decrease in -electron density on the ring containing the substituent, which corresponds to an increase in the -dipole between the two rings. An examination of the solution structures of the - complexes formed by amodiaquine and quinine with heme (Leed et al. Biochemistry 2002, 41, 10245. de Dios et al. Inorg. Chem. 2004, 43, 8078) shows that the ...
Chloroquine (CQ), a 4-aminoquinoline, accumulates in acidic digestive vacuoles of the malaria parasite, preventing conversion of toxic haematin to beta-haematin. We examine how bis 4-aminoquinoline piperaquine (PQ) and its hydroxy-modification (OH-PQ) retain potency on chloroquine-resistant (CQ-R) Plasmodium falciparum. For CQ, PQ, OH-PQ and 4 and 5, representing halves of PQ, beta-haematin inhibitory activity (BHIA) was assayed, while potency was determined in CQ-sensitive (CQ-S) and CQ-R P. falciparum. From measured pK(a)s and the pH-modulated distribution of base between water and lipid (logD), the vacuolar accumulation ratio (VAR) of charged drug from plasma water (pH 7.4) into vacuolar water (pH 4.8) and lipid accumulation ratio (LAR) were calculated. All agents were active in BHIA. In CQ-S, PQ, OH-PQ and CQ were equally potent while 4 and 5 were 100 times less potent. CQ with two basic centres has a VAR of 143,482, while 4 and 5, with two basic centres of lower pK(a)s have VARs of 1287 and ...
The development of new CH functionalization protocols based on inexpensive cobalt catalysts is currently attracting significant interest. Functionalized 8-aminoquinoline compounds are high-potential building blocks in organic chemistry and pharmaceutical compounds and new facile routes for their preparation would be highly valuable. Recently, copper has been applied as catalyst for the functionalization of 8-aminoquinoline compounds and found to operate through a single electron transfer (SET) mechanism, although requiring elevated reaction temperatures. Herein, we described the first example of a cobalt-catalyzed remote CH functionalization of 8-aminoquinoline compounds operating through a SET mechanism, exemplified using a practical and mild nitration protocol. The reaction uses inexpensive cobalt nitrate hexahydrate [Co(NO3)2⋅6 H2O] as catalyst and tert-butyl nitrite (TBN) as nitro source. This methodology offers the basis for the facile preparation of many new functionalized ...
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Information about using Aldara cream to treat three different skin conditions: genital warts, small superficial skin cancers and actinic keratoses.
IMIQUIMOD, 1 INDICATIONS AND USAGE Aldara Cream is indicated for the topical treatment of: •Clinically typical, nonhyperkeratotic, nonhypertrophic actinic keratoses (AKs) on the face or scalp in immunocompetent
Treatment: ALDARA from your local pharmacy. 1.Apply 3 times per week (such as Monday, Wednesday, and Friday) for no longer than 16 weeks. 2. Apply the cream from one Aldara packet to the treatment area, and rub in the cream until it disappears. 3. Do not cover the treated skin areas with any type of plastic bandaging, and avoid nylon underwear. 4. You may wear cotton gauze or underwear over the treated area. 5. Use the medicine before going to bed and leave it on for 6 to 10 hours. Then wash off the medicine with water and a mild soap.. 6. When treating genital warts around the vagina, avoid getting the cream on the more sensitive inner layers of vaginal tissue. This could result in vaginal swelling or irritation and painful urination.. 7. Aldara is not a cure for molluscum or genital warts and it may not keep you from spreading this condition to others through vaginal, anal, or oral sex. You may develop new lesions during treatment with Aldara. ...
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Vyloma: Imiquimod cream belongs to a group of medications called immune response modifiers. It works by stimulating the bodys defenses to fight certain types of skin conditions. Imiquimod cream is used to treat external genital and perianal warts caused by the human papillomavirus (HPV) in adults. The external genital area includes skin surfaces on and around the vagina or penis. The perianal area includes skin surfaces surrounding the anus (the opening through which fecal matter is passed).
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Toll-like receptor (TLR)-mediated signaling induces cell migration or invasion in several tumors and various stages of cancer. Interactions of mesothelin, a 40-kDa cell surface glycoprotein, with cancer antigen 125 (CA125) is associated with drug resistance, metastasis, and poor clinical outcome of ovarian cancer patients. In this study, we examined the role of TLR5 and TLR7 in the metastasis of ovarian cancer through the induction of mesothelin/CA125 expression and investigated its underlying mechanism. TLR5 agonist (flagellin) and TLR7 agonist (imiquimod) upregulated mesenchymal phenotypes and produced epithelial-mesenchymal transition (EMT)-related cytokines in the SKOV3 cells; however, TLR7 expressing CaOV3 cells had no response to the specific ligand, imiquimod, for enhancing its EMT processes ...
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Pharmaceutical formulations and methods including an immune response modifier (IRM) compound and an oleic acid component are provided where stability is improved by using oleic acid have low polar impurities such as peroxides.
Pharmaceutical formulations and methods including an immune response modifier (IRM) compound and an oleic acid component are provided where stability is improved by using oleic acid have low polar impurities such as peroxides.
Pharmaceutical formulations and methods including an immune response modifier (IRM) compound and an oleic acid component are provided where stability is improved by using oleic acid have low polar impurities such as peroxides.
The cyclization of 3-N(4- and 5-benzimidazolyl and benztriazolyl)amino-2-cyano- and 2-ethoxycarbonyl-2-propenoate esters Ia, b-IVa, b under the conditions of the Gould-Jacobs reaction leads to angularly ring-fused substituted imidazo or triazolo[4,5-f] (V, VI) and [4,5-h] (VII, VIII) quinolines, respectively. The esters Vb-VIIIb have been transformed into the corresponding chloroderivatives Vc-VIIIc. 3-N(5-Benzimidazolyl and 5-benztriazolyl)amino-2-cyano-2-propenenitriles are cyclized in the presence of aluminium(III) chloride to give the aminoquinolines Vd, VId. The structure of the products has been characterized by their 1H, 13C NMR, IR, and UV spectra.. ...
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Imiquimod is a medication successfully used in the treatment of skin diseases. In addition to its known mechanism of action, it also triggers other processes in the body. Scientists at the Technical University of Munich (TUM) have succeeded in explaining the molecular fundamentals of these additional effects. The results also shine a new light on other known molecular processes which could indicate an approach to the treatment of inflammatory illnesses.
K. 34, each imiquimod cost canada element was modulated between stimulus A Imiquimгd consecutive dark frames followed by eight consecutive light frames) and stimulus B (16 consecutive dark frames) according to a binary m-sequence. Second, the symptoms resolved after dialysis.
When using imiquimod, the dosing instructions will depend on the condition being treated and other factors. This eMedTV resource presents a brief description of how your treatment plan will be determined. This page also links to more detailed information.
Hazen PG, Carney JF, Engstrom CW, Turgeon KL, Reep MD, Tanphaichitr A. Proliferating Hemangioma of Infancy: Successful Treatment with Topical 5% Imiquimod Cream. Pediatr Dermatol. 2005 May-Jun;22(3):254-6 ...
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JTC-801 je opioidni analgetik koji se koristi u naučnim istraživanjima.[1][2]. JTC-801 je selektivni antagonist nociceptinskog receptora.[3] U hronološkom redu otkrića to je bio četvrti opioidni receptor. On je još uvek najmanje istražen. Nociceptinski receptor proizvodi kompleksne efekte koji učestvuju u mnogim procesima vezanim za bol i inflamaciju. Aktivacija ovog receptora može bilo da povisi ili umanji bol u zavisnosti od doze.[4] Lekovi koji deluju na nociceptinski receptor mogu da imaju uticaj na dejstvo tradicionalnih analgetika kao što su inhibitori prostaglandinske sintetaze (NSAID),[5] μ-opioidne agoniste,[6] i kanabinoide.[7]. JTC-801 je oralno aktivni lek koji blokira nociceptinski receptor i proizvodi analgetske efekte u nizu studija na životinjama. On je posebno koristan u kontroli neuropatskog bola i alodinije vezanih za ozlede nerva.[8][9][10]. ...
I have had an area of concern (to me) on my nose for over 3 years. Have been to the dermatologist numerous times during this period and she said it was nothing. I finally insisted on a biopsy and it came back as superficial basal cell. They are recommending Mohs surgery but I am nervous about it as it is in a location (right side tip) that could possibly require extensive reconstruction surgery. I had a consult with the surgeon this weekend and he said the lesion appears small and probably wouldnt require reconstruction (forehead flap) but wouldnt know for sure until they did the surgery. I asked about using Aldara and both my dermatologist and Mohs surgeon agreed I could try that and then be reevaluated after that treatment.. Now Im reading all the scary reviews of bad side effects online for Aldara. Cant decide if I should just do the Mohs or try the Aldara.. I had Mohs 13 years ago (also on my nose but on the far side-2 passes). The closure was just 7 stitches and no scars left ...
Pini, A M; Koch, S; Schärer, L; French, L E; Läuchli, S; Hofbauer, G F L (2008). Eruptive keratoacanthoma following topical imiquimod for in situ squamous cell carcinoma of the skin in a renal transplant recipient. Journal of the American Academy of Dermatology, 59(5):S116-S117. ...
Zyclara 3.75% Creme Sachets 28 ST für 162,70 Euro (23.04.2016). 4 Preise im Preisvergleich. Das Präparat enthält den Wirkstoff Imiquimod.. ❸-3-6}. Define perianal warts. perianal warts synonyms,. FDA Approves Zyclara[R] (imiquimod) Cream, 3.75% for the Treatment of External Genital Warts.ZYCLARA 3,75% Creme Sachets 28 Stück Artikelnummer:. 9,375 mg Imiquimod + Isostearinsäure + Benzylalkohol. 5,5 mg Cetylalkohol. 7,75 mg Stearylalkohol + Vaselin.Graceway Pharmaceuticals has received US Food and Drug Administration approval for Zyclara (imiquimod) cream, 2.5% for the treatment of actinic keratoses.Zyclara™Cream imiquimod 3.75% Imiquimod is on the formulary. *Physicians may request coverage of these products using the Prescription Drug Medication Request Form ...
Psoriasis is a chronic inflammatory skin disease with a strong genetic background and is triggered by environmental factors. Available evidence supports CD6, a lymphocyte surface receptor mostly expressed by T cells, as a putative target in autoimmunity. Accordingly, a humanized anti-CD6 antibody has been assayed for the treatment of certain autoimmune disorders, including psoriasis. Here, we present novel evidence in mice and humans for a direct involvement of CD6 in psoriasis pathophysiology. First, an attenuated form of imiquimod-induced psoriasis-like skin inflammation was demonstrated in CD6-deficient mice, as deduced from lower epidermal thickness and local reduced production of pro-inflammatory cytokines, namely, interleukin-17A ...
Melanoma is the most serious type of skin cancer as a malignant tumor of melanocytes. Metastatic melanoma can be fatal with the 5-year survival rate below 15% and median survival of about 6-8 months.1 Due to the development of metastatic disease which is highly resistant to conventional chemotherapeutics and radiation, the intensive research and effort into new drugs and treatments2 afforded merely the response rates of approximately 20% or less. We report here the synthesis of a novel series of aminoquinoline derivatives 1a-p based on the structural features of Sorafenib (Nexavar)3 (Figure 1) and their antiproliferative activities and selectivities against human melanoma cell line and fibroblast cell line ...
A novel and efficient regioselective C-H fluorination of 8-aminoquinoline amides and sulfonamides at C5 position was achieved. Using selectfluor as
Topical chemotherapy is applied with a cream such as Efudex (5-fluorouracil), Carac (5-fluorouracil),or Aldara (imiquimod). It is a highly effective treatment for pre-cancerous lesions such as Actinic Keratoses (AK). As an alternative treatment to surgery, topical chemotherapy can treat some superficial Basal Cell carcinomas (BCCa) and superficial Squamous Cell carcinomas (SCCa). This treatment is best reserved for early superficial skin cancers and can be unpredictable. 5-fluorouracil creams such as Efudex and Carac are the real chemotherapeutic drugs, killing abnormal cells directly. Imiquimod (Aldara) works differently by summoning forth immune cells that do the killing. It is called an immune response modifier. Imiquimod has also been applied to other skin cancers such as Bowens carcinoma in-situ and melanoma in-situ. An appointment with your physician will help to determine the answer to this question. Not all forms of skin cancer can be treated with the use of topical chemotherapy. The ...
Participants will be required to come to the hospital for examinations on Week 1, 2, 4 and 6 (+/- 3 calendar days) and after their last dose of imiquimod cream on Weeks 9, 12 and 18 (+/- 5 calendar days. The following tests and procedures will be performed: skin test; vital signs and measurements and photographs of the tumors. Participants will be asked to participate in an optional skin biopsy on Week 4 and research blood tests wil lbe taken on Day 1 ...
1 Answer - Posted in: aldara, basal cell carcinoma, cancer, lips, cream - Answer: Bernie, The physician, hope an oncologist, that prescribed that ...
Imiquimod is an immune response modifier. Imiquimod topical is used to treat actinic keratosis (a condition caused by too much sun exposure) on the face and scalp. Imiquimod topical (for the skin) is also used to treat a minor form of skin cancer called superficial basal cell carcinoma, when surgery would not be an...
Informed choice is of ethical and practical importance in mammography screening. To assess the level to which decisions regarding such screening are informed is thus imperative, but no specific instrument has been available to measure informed choice in the German mammography screening programme. The aims of this study were to develop the Informed Choice in Mammography Screening Questionnaire (IMQ) and to find first evidence for the factor structure, reliability and validity of its different components. The IMQ was sent to 17.349 women aged 50 in Westphalia-Lippe, Germany. The instrument has been developed after consideration of (1) the results of qualitative interviews on decision making in the mammography screening programme, (2) relevant literature on other informed choice instruments and (3) a qualitative study on influencing factors. The IMQ comprises 3 scales (attitude, norms, and barriers), 1 index (knowledge) and singular items covering intention to participate and sociodemographic variables. To
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Imiquimod - Get up-to-date information on Imiquimod side effects, uses, dosage, overdose, pregnancy, alcohol and more. Learn more about Imiquimod
Orf is a self-limiting disease, which means it will get better on its own without treatment. It usually clears up within three to six weeks. It may be useful to cover the lesion with a sterile (hygienic) dressing and immobilise your finger to help reduce discomfort. Read more about applying plasters and other dressings.. You should see your GP if the lesion isnt healing, you develop a fever (high temperature) or youre in severe pain, as some people also develop a bacterial infection. This may require treatment with antibiotics. In rare cases the lesion may not go away and a minor surgical procedure may be required to remove it.. Although theres some evidence to suggest that using topical imiquimod cream may help to reduce lesions, you should speak to your GP or pharmacist for advice first.. ...
Hi fifi65 and welcome to the online community. I havent had this treatment but noticed your post hadnt had any replies yet. Im sorry to hear how painful youre finding using Aldara (Imiquimod) cream is.. You should have been given a leaflet from you hospital when they prescribed this treatment telling you how to apply it and what to expect. I dont know which hospital you attended but have found this information from Royal Berkshire Hospital for you if you havent been given any information. The leaflet says to be guided by how severely you react and to stop using it if your reaction is severe and you are unable to tolerate it. However, its important to use the cream as your hospital prescribed it.. If you have had a severe reaction to the cream then Id recommend getting in touch with your team as soon as possible so that they can advise you what to do.. x ...
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Like a tourist without a map, tumor-fighting T cells have a hard time finding their destination without directions. According to Clark et al. (page 2221), dismantling these directions helps skin cancer cells hide from killer T cells.. To enter the skin, T cells must grab on to the adhesive molecule E-selectin, which is expressed on the endothelial cells lining blood vessels in the skin. The authors now find that many of the vessels in skin cancer lesions lack E-selectin, causing beneficial T cells to pass by unaware. The tumors were instead populated by suppressive regulatory (T reg) cells, perhaps coaxed in by the tumor to safeguard against killer cells that somehow gain access. Both tactics have also been seen in other types of human cancer.. Reversing the suppressive effect of T reg cells is one of the beneficial effects of topical immune-stimulating drugs like the TLR agonist imiquimod, which is effective in treating certain types of skin cancer. Indeed, Clark et al. found that imiquimod ...
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Type I hypersensitiv- ity requires previous exposure to the specific antigen. ). Appl. Reading with multiple preferred retinal loci implications for training a more efficient reading strategy.
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The six reviews in this volume cover once again a most comprehensive range of topics. The anti-malarial activity of the 8-aminoquinolines is examined, with an eye to the development of a single, broad-spectrum drug. Chelation, important in removal of toxic metals from the body, is reviewed for tripositive elements. A new and promising approach to total parenteral nutrition is described. Our indebtedness to the plant origins of many modern drugs is noted in the context of new chemicals. Heterosteroids and receptor-specific opioid peptides constitute two further topics, each case highlighting the wide range of relevant biologically active compounds. Yet another volume challenging the staggering diversity of the field of medicinal chemistry ...
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A 4-aminoquinoline with antimalarial and immunosuppressive properties. Although its precise mechanism of action is unknown, hydroxychloroquine may suppress immune function by interfering with the processing and presentation of antigens and the production of cytokines. This agent is highly active against the erythrocytic forms of P. vivax and malariae and most strains of P. falciparum but not the gametocytes of P. falciparum. Check for "http://www.cancer.gov/Search/ClinicalTrialsLink.aspx?id=38571&idtype=1″ active clinical trials or "http://www.cancer.gov/Search/ClinicalTrialsLink.aspx?id=38571&idtype=1&closed=1″ closed clinical trials using this agent. ("http://nciterms.nci.nih.gov:80/NCIBrowser/ConceptReport.jsp?dictionary=NCI_Thesaurus&code=C557″ NCI Thesaurus ...
Although you dont indicate what your CD4 count, percent and HIV viral load are, or changed to, it is unlikely the aldara cream caused the very mild decrease in...
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Imiquimod 3.75% cream has recently been approved by both the U.S. Federal Drug Administration and Health Canada for the treatment of external genital warts. Herein, we provide an overview of external genital warts, review the phase 3 clinical trials leading to the approval of imiquimod 3.75% cream, and compare its efficacy and clinical use with imiquimod 5% cream...
Another common use of imiquimod is for the treatment of squamous cell carcinoma in situ (Bowens disease). It is best to apply imiquimod prior to bedtime and leave it on the affected area for 6-10 hours. Imiquimod can be removed from the skin by gently washing the area with mild soap and water. Always use caution when applying imiquimod to areas near the mouth, nose or eyes. Additionally, do not apply imiquimod to any area of the body other than the prescribed area. In certain situations your physician may recommend a rest period, at which time imiquimod should be discontinued until the local inflammation has subsided.. Side Effects: The overwhelming majority of patients using imiquimod develop side effects. The most common side effects include irritant contact dermatitis, redness, swelling, burning sensation, pain, tenderness and flaking, peeling or crusting at the application site. Although these secondary responses can be startling, some research has suggested that the greater the ...
Pneumocystis pneumonia (PCP) is one of the most frequent causes of mortality among HIV-infected patients. Primaquine (PQ) is an antimalarial 8-aminoquinoline effective against PCP when given in combination with clindamycin. This has drawn the attention of Medicinal Chemists towards the anti-PCP activity of 8-aminoquinolines, not only confined to those exhibiting antimalarial activity [1]. It is thought that anti-PCP 8-aminoquinolines exert their anti-PCP activity by acting on the electronic transport and redox system of the P. carinii pathogen [1]. Recently, our research group has been developing imidazolidin-4-one derivatives of PQ (Scheme 1), targeting novel compounds with improved therapeutic action, namely, higher resistance to metabolic inactivation, lower toxicity and equal or higher antimalarial activity than that of the parent drug [2,3]. These imidazolidin-4-ones were seen to block the transmission of rodent malaria, caused by Plasmodium berghei on BalbC mice, to the mosquito vector ...
Well after almost 12 months of anguish, various treatments and no PE my warts have finally gone. After the usual 4 months of keeping it quiet I plucked up the courage to visit my GP who prescribed Aldara cream. Several months of this resulted in limited success. A particularly stubborn cluster meant a referral to a consultant urologist who used stuff called Trichloro Acetic Acid. This burned like the fires of hell, but boy did it obliterate the stubborn warts! After several doses of this stuff and some mopping up with Aldara (which seemed to work better on the treated warts as the skin became more permeable) Im finally clear and back on full PE routine. I know that I will have the virus for life and outbreaks of warts are always possible, but I now have a strategy for dealing with them - hit them early with Aldara, roughen the surface with an emery board (or even cut them off!) and work the cream into the softened surface - gone in 2 days! It feels so good to be back at this wonderful quest for ...
Abstract This report summarizes the results of experimental studies that underpinned evaluation of primaquine in human volunteers inoculated with sporozoites of the Chesson strain of Plasmodium vivax and current uses of this 8-aminoquinoline for curative and preventive purposes. These experimental studies dealt with both the curative and prophylactic activities of selected 8-aminoquinolines in rhesus monkeys infected or challenged with sporozoites of P. cynomolgi and the toxicities of these agents for non-infected monkeys. They began with preliminary assessments of the curative activities and toxicities of five 6-methoxyquinolines differing from each other with respect to alkyl substituent in the 8-aminoal-kylamino side chain. Primaquine, one of these five derivatives, was the most active and had the best therapeutic index. Results of expanded evaluations of its curative activity and toxicity, compared with results of earlier appraisals of the activities and toxicities of pamaquine, pentaquine, and
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In chronic diseases, such as HIV infection, plasmacytoid dendritic cells (pDCs) are rendered dysfunctional, as measured by their decreased capacity to produce IFN-α. In this study, we identified elevated levels of T cell Ig and mucin-domain containing molecule-3 (Tim-3)-expressing pDCs in the blood of HIV-infected donors. The frequency of Tim-3-expressing pDCs correlated inversely with CD4 T cell counts and positively with HIV viral loads. A lower frequency of pDCs expressing Tim-3 produced IFN-α or TNF-α in response to the TLR7 agonists imiquimod and Sendai virus and to the TLR9 agonist CpG. Thus, Tim-3 may serve as a biomarker of pDC dysfunction in HIV infection. The source and function of Tim-3 was investigated on enriched pDC populations from donors not infected with HIV. Tim-3 induction was achieved in response to viral and artificial stimuli, as well as exogenous IFN-α, and was PI3K dependent. Potent pDC-activating stimuli, such as CpG, imiquimod, and Sendai virus, induced the most ...
Clinical Question: Is imiquimod (Aldara) 5 percent cream safe and effective for the treatment of actinic keratoses (AKs)?. Setting: Outpatient (specialty). Study Design: Randomized controlled trial (double-blinded). Synopsis: As the ozone layer thins and as we live longer and have more leisure time for outdoor recreation, it is not surprising that we have more and more AKs. These traditionally have been frozen off or treated with curettage, topical fluorouracil, or even chemical peels. Imiquimod is an oddly named immune-response modifier that has anecdotally shown promise in the treatment of AKs.. In this manufacturer-sponsored study, otherwise healthy adults older than 45 years with three to 10 AKs were randomized to receive treatment with imiquimod 5 percent cream or vehicle cream. The cream was applied three times per week for eight hours at a time (left on overnight) for a total of 12 weeks. Masking of patients, physicians, and outcome assessors was appropriate, as was allocation ...
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The present invention relates to novel improvements in the chemotherapy of malaria, consisting in the development of new primaquine analogues which exhibit practical levels of effectiveness in experimental malaria both when induced by sporozoites of infectious Plasmodia and by introduction of infectious trophozoites of the parasites. Such range of chemotherapeutic effectiveness against forms of the malaria parasite both in tissues and in blood affords a unique melding of worth especially because achieved without the gross liability of hazardous toxic side-effects otherwise characteristic of 8-aminoquinolines. In truth, such new primaquine analogues provide a remarkably broad spectrum of antimalarial activity in relation to the life cycle of the parasite. Practical utility of the class as being both clinically curative and radically curative antimalarials is envisioned.*PATENTS
TY - JOUR. T1 - Treatment of actinic cheilitis with imiquimod 5% and a retractor on the lower lip. T2 - British Journal of Oral and Maxillofacial Surgery. AU - McDonald,Christopher. AU - Laverick,Sean. AU - Fleming,Colin J.. AU - White,Sharon J.. PY - 2010/9. Y1 - 2010/9. N2 - Imiquimod 5% (Aldara (TM), 3M Healthcare Ltd.) is a topically applied immune response modifier used in the treatment of superficial basal cell carcinoma, actinic keratosis, and genital warts. We reviewed the casenotes of 5 patients with histologically confirmed dysplastic lower lips who had been treated with topical imiquimod.Each patient was provided with a specially designed lower lip retractor to prevent spread of the cream. Treatment was stopped after 6 weeks or if an acute inflammatory reaction developed. The lower lip was biopsied 4 weeks later, and histologically the dysplastic changes had been reversed in all 5 patients. The lip retractor was well-tolerated, and prevented spread of the cream. Imiquimod 5% cream ...
We conducted a review of the effects of adding a single dose (or short course) of primaquine to malaria treatment with the aim of reducing the transmission of malaria. We included 17 randomized controlled trials and one quasi-randomized controlled trial.. What is primaquine and how might it reduce transmission. Primaquine is an antimalarial drug which does not cure malaria illness, but is known to kill the gametocyte stage of the malaria parasite which infects mosquitoes when they bite humans. Primaquine is also known to have potentially serious side effects in people with an enzyme deficiency common in many malaria endemic settings (glucose-6-phosphate dehydrogenase (G6PD) deficiency). In these people, high doses of primaquine given over several days sometimes destroys red blood cells, causing anaemia and, in some cases, possibly life-threatening effects.. The World Health Organization (WHO) recommends adding a single dose of primaquine to malaria treatment with the intention of reducing ...
A 44-year-old man who was previously diagnosed with actinic cheilitis was prescribed imiquimod cream 5%, which resulted in thick hemorrhagic crusting of the lower lip after 4 applications. He subsequently noted the development of lichen planus lesions on his arms and legs for the first time in 15 years following imiquimod use. On follow-up he also was noted to have characteristic Wickham striae on his lower lip. Lichen planus is an autoimmune inflammatory condition in which autoreactive T lymphocytes attack keratinocytes. The mechanism of action for imiquimod is upregulation of IFN-alpha and IFN-beta. Treatment with clobetasol cream 0.05% led to resolution of his lichen planus lesions.
Part 1 of this series provided some background to the Australian Army Malaria Institutes (AMI) tafenoquine trials in 1999-2002, including an outline of the preceding trials and more recent laboratory studies relating to the drugs efficacy and toxicity. This post provides a more detailed examination of the chronology of the trials and the numbers of…
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What causes Bowens disease? Most cases of Bowens disease develop as a result of long-term sun exposure. Very occasionally, Bowens disease may be seen in the context of previous radiotherapy, following chronic arsenic ingestion (very rare nowadays) or on the genitalia in association with the virus that causes warts (the human papillomavirus). Bowens disease is neither infectious, nor due to an allergy. Is it hereditary? No, but some of the factors that increase the risk of getting it, such as a fair skin and a tendency to burn in the sun, do run in families. What are its symptoms? Often there are no symptoms, although the surface crusting may catch on clothing. What does it look like? A patch of Bowens disease starts as a small red scaly area, which grows very slowly. It may reach a diameter of a few centimetres across. It commonly occurs on sun-exposed skin, especially the head, hands and lower legs. More than one lesion may be present. The development of an ulcer or lump on a patch of ...

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ANALYSIS OF PLASMODIUM FALCIPARUM CHLOROQUINE RESISTANCE TRANSPORTER ISOFORMSANALYSIS OF PLASMODIUM FALCIPARUM CHLOROQUINE RESISTANCE TRANSPORTER ISOFORMS

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8-Aminoquinoline 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 ... The 8-aminoquinoline drugs must not be given to patients with G6PD deficiency, because they cause potentially fatal haemolysis ... "Short report: The activity of pamaquine, an 8-aminoquinoline drug, against sporozoite-induced infections of Plasmodium vivax ( ...
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3-Aminoquinoline 0.98; CAS No.: 580-17-6; Synonyms: 3-AQ; 3-Quinolinamine; Linear Formula: C9H8N2; Empirical Formula: C9H8N2; ... 3-Aminoquinoline was used:. • in liquid matrix for matrix-assisted laser desorption/ionization mass spectrometry (MALDI-MS) for ...
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5-Aminoquinoline 99.0 %, TCI America 5G Chemicals:Organic Compounds:Organoheterocyclic compounds:Quinolines and derivatives: ... 5-aminoquinoline,5-quinolinamine,quinoline, 5-amino,5-quinolylamine,quinolin-5-ylamine,unii-yyj34z13sh,5-amino-quinoline,ccris ... 5-aminoquinoline,5-quinolinamine,quinoline, 5-amino,5-quinolylamine,quinolin-5-ylamine,unii-yyj34z13sh,5-amino-quinoline,ccris ...
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WO2018196823 2-AMINO-QUINOLINE DERIVATIVESWO2018196823 2-AMINO-QUINOLINE DERIVATIVES

EN) 2-AMINO-QUINOLINE DERIVATIVES. (FR) DÉRIVÉS DE 2-AMINO-QUINOLÉINE. Abstract: (EN) Described herein are 2-amino-quinoline ... in need thereof by administering a therapeutically effective amount of a 2-amino-quinoline derivative.. (FR) Linvention ...
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Depending upon the location of the amino group, they can be divided into: 4-Aminoquinoline 8-Aminoquinoline. ... Aminoquinolines are derivatives of quinoline, most notable for their roles as antimalarial drugs. ...
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4-Aminoquinoline is a form of aminoquinoline with the amino group at the 4-position of the quinoline. A variety of derivatives ... Bourne SA, De Villiers K, Egan TJ (2006). "Three 4-aminoquinolines of antimalarial interest". Acta Crystallogr C. 62 (Pt 2): ... Amodiaquine Chloroquine Hydroxychloroquine Bray PG, Hawley SR, Ward SA (1996). "4-Aminoquinoline resistance of Plasmodium ... of 4-aminoquinoline are antimalarial agents useful in treating erythrocytic plasmodial infections. Examples include amodiaquine ...
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The American Journal of Tropical Medicine and Hygiene | A Role for 8-Aminoquinolines in Falciparum Malaria?The American Journal of Tropical Medicine and Hygiene | A Role for 8-Aminoquinolines in Falciparum Malaria?

Much attention was paid to the apparent absence of 4-aminoquinoline resistance in much of Central America (less Panama) and in ... There was considerable discussion of Plasmodium falciparum resistance to the 4-aminoquinolines and to mefloquine. The ... A Role for 8-Aminoquinolines in Falciparum Malaria? * Author(s): * Publisher: The American Society of Tropical Medicine and ... Much attention was paid to the apparent absence of 4-aminoquinoline resistance in much of Central America (less Panama) and in ...
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It is based upon the use or administration of therapeutically effective amount of certain 8-aminoquinoline compositions which ... It is based upon the use or administration of therapeutically effective amount of certain 8-aminoquinoline compositions which ... Title : Method for Inducing Protection in Animal Against Cyanide Poisoning Using 8-Aminoquinolines. ...
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5-Position-selective C-H trifluoromethylation of 8-aminoquinoline derivatives - Organic & Biomolecular Chemistry (RSC...5-Position-selective C-H trifluoromethylation of 8-aminoquinoline derivatives - Organic & Biomolecular Chemistry (RSC...

We developed a copper-catalyzed 5-position-selective C-H trifluoromethylation of 8-aminoquinoline derivatives. The reaction ... 5-Position-selective C-H trifluoromethylation of 8-aminoquinoline derivatives Y. Kuninobu, M. Nishi and M. Kanai, Org. Biomol. ... On the other hand, the trifluoromethylation of 8-aminoquinolines was also promoted by other Lewis acids as well as a copper ... These results indicated that the trifluoromethylation of 8-aminoquinolines proceeded via a Friedel-Crafts-type reaction. ...
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2,6-dimethyl-N-[(2-oxo-1-propyl-indol-3-ylidene)amino]quinoline-4-carboxamide2,6-dimethyl-N-[(2-oxo-1-propyl-indol-3-ylidene)amino]quinoline-4-carboxamide

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NY D87815 - The tariff classification of 8-Aminoquinoline (CAS 578-66-5) from China and Tricyclic Olefin from Italy. - United...NY D87815 - The tariff classification of 8-Aminoquinoline (CAS 578-66-5) from China and Tricyclic Olefin from Italy. - United...

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Plasmodium Falciparum Malaria in Panama Resistant to 4-Aminoquinoline Drugs* | The American Journal of Tropical Medicine and...Plasmodium Falciparum Malaria in Panama Resistant to 4-Aminoquinoline Drugs* | The American Journal of Tropical Medicine and...

This is the first report of 4-aminoquinoline drug resistance in P. falciparum malaria in a country north of Colombia in the ... 4-aminoquinoline drugs. The cure rate was only 22%. Failures were represented by relapses, persistence of the parasitemia, or ... Plasmodium Falciparum Malaria in Panama Resistant to 4-Aminoquinoline Drugs * * Martin D. Young, Carl M. Johnson ... This is the first report of 4-aminoquinoline drug resistance in P. falciparum malaria in a country north of Colombia in the ...
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Exploring QSAR for Antimalarial Activities and Drug Distribution within Blood of a Series of 4-Aminoquinoline Drugs Using...Exploring QSAR for Antimalarial Activities and Drug Distribution within Blood of a Series of 4-Aminoquinoline Drugs Using...

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In Vivo and In Vitro Efficacy of Amodiaquine against  Plasmodium falciparum  in an Area of Continued Use of 4-Aminoquinolines...In Vivo and In Vitro Efficacy of Amodiaquine against Plasmodium falciparum in an Area of Continued Use of 4-Aminoquinolines...

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A novel and efficient regioselective C-H fluorination of 8-aminoquinoline amides and sulfonamides at C5 position was achieved. ... C5-regioselective C-H fluorination of 8-aminoquinoline amides and sulfonamides with selectfluor under metal-free conditions ... C5-regioselective C-H fluorination of 8-aminoquinoline amides and sulfonamides with selectfluor under metal-free conditions Y. ... A novel and efficient regioselective C-H fluorination of 8-aminoquinoline amides and sulfonamides at C5 position was achieved. ...
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6-Acylamino-2-aminoquinolines as potent melanin-concentrating hormone 1 receptor antagonists. Identification, structure...6-Acylamino-2-aminoquinolines as potent melanin-concentrating hormone 1 receptor antagonists. Identification, structure...

6-Acylamino-2-aminoquinolines as potent melanin-concentrating hormone 1 receptor antagonists. Identification, structure- ... 6-Acylamino-2-aminoquinolines as potent melanin-concentrating hormone 1 receptor antagonists. Identification, structure- ... 6-Acylamino-2-aminoquinolines as potent melanin-concentrating hormone 1 receptor antagonists. Identification, structure- ... Novel 6-acylamino-2-aminoquinoline melanin-concentrating hormone 1 receptor (MCH1R) antagonists were identified by sequential ...
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The aminoquinoline - pyrazinamide hybrid N-(2-((7-chloroquinolin-4-yl)amino)ethyl)pyrazine-2-carboxamide and its complexes with ... The most successfully deployed aminoquinoline anti-malarial drug is chloroquine, see Fig. 1. It was used massively on a global ... The synthesis and characterization of N-(2-((7-chloroquinolin-4-yl)amino)ethyl)pyrazine-2-carboxamide (L), an aminoquinoline - ... In this study, we have set out to investigate the possibilities of aminoquinoline hybrids with pharmacophores from tuberculosis ...
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  • It is based upon the use or administration of therapeutically effective amount of certain 8-aminoquinoline compositions which are administered orally. (dtic.mil)
  • This assay was used to screen a series of 18 known antimalarials and 14 new non 8-aminoquinolines (preselected for blood and/or liver stage activity) in three-point tenfold dilutions (0.1, 1 and 10 µM final concentrations). (novartis.com)
  • This parasite requires the use of 8-aminoquinoline drugs to prevent relapses from liver hypnozoites, but high prevalence of glucose-6-phosphate dehydrogenase deficiency in the endemic human populations makes it difficult to adopt this treatment regimen. (intechopen.com)