Results 221 to 230 of about 340,090 (253)
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THE EFFECT OF CYCLOOXYGENASE-2 INHIBITORS ON SPINAL FUSION
The Journal of Bone and Joint Surgery-American Volume, 2002Spine surgeons discourage the use of nonsteroidal anti-inflammatory drugs following spine arthrodesis because of their inhibitory effect on bone-healing. To our knowledge, there are no data on the effects of the new cyclooxygenase-2 inhibitors on bone-healing.
John, Long +4 more
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Inhibiting HIV-1 Entry with Fusion Inhibitors
Current Medicinal Chemistry, 2003In recent years, tremendous progress has been made in understanding the HIV-1 entry process in which the viral and cellular membranes are fused, resulting in the subsequent delivery of the viral genome into the host cell. The mechanistic insight gained from these studies has led to the formulation of exciting new approaches for therapeutic intervention.
C E, Baldwin, R W, Sanders, B, Berkhout
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The fusion inhibitor enfuvirtide in recent antiretroviral strategies
Current Opinion in HIV and AIDS, 2009The purpose of this review is to discuss recent pharmacological, virological, and clinical data that concern enfuvirtide usage in different antiretroviral combinations.Randomized, recent trials in multidrug-experienced patients suggest that antiretroviral combinations with enfuvirtide have excellent virological responses with new antiretroviral ...
Alain, Makinson, Jacques, Reynes
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Novel quinolizidine salicylamide influenza fusion inhibitors
Bioorganic & Medicinal Chemistry Letters, 1999A novel series of quinolizidine salicylamides was synthesized as specific inhibitors of the H1 subtype of influenza A viruses. These inhibitors inhibit the pH-induced fusion process, thereby blocking viral entry into host cells. Compound 16 was the most active inhibitor in this series with an EC50 of 0.25 microg/mL in plaque reduction assay.
K L, Yu +11 more
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The introduction of the fusion inhibitors in the HAART-regimens.
The new microbiologica, 2004Interference with HIV entry into target cells provides a novel approach to the treatment of HIV infection. The inhibition of virus fusion with the co-receptor substrate seems the most specific and potentially best way to interfere with HIV infection and replication.
Hasson H +5 more
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IDrugs : the investigational drugs journal, 2003
The majority of current antiviral drugs target viral genome replication (eg, reverse transcriptase inhibitors) or virion maturation (eg, protease inhibitors). Although efficient, these drugs suffer from the quick appearance of drug-resistant mutants and usually do not eliminate the virus completely.
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The majority of current antiviral drugs target viral genome replication (eg, reverse transcriptase inhibitors) or virion maturation (eg, protease inhibitors). Although efficient, these drugs suffer from the quick appearance of drug-resistant mutants and usually do not eliminate the virus completely.
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Peptide and Non-peptide HIV Fusion Inhibitors
Current Pharmaceutical Design, 2002Fusion of the HIV envelope with the target cell membrane is a critical step of HIV entry into the target cell. The HIV envelope glycoprotein gp41 plays an important role in the fusion of viral and target cell membranes and serves as an attractive target for development of HIV fusion inhibitors.
Shibo, Jiang +2 more
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Development of HIV-1 Fusion Inhibitors Targeting gp41
Current Medicinal Chemistry, 2014The HIV-1 envelope protein glycoprotein 41 (gp41) is crucial in the HIV-1 infection process, therefore gp41 has emerged as an attractive target for drug design against AIDS. During the past few decades, tremendous efforts have been made on developing inhibitors that can prevent the HIV-1 entry process via suppressing functional gp41.
Lu, K. +3 more
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[Integrase inhibitor, CCR5 antagonist, fusion inhibitor].
Nihon rinsho. Japanese journal of clinical medicine, 2010Integrase inhibitors have a novel antiretroviral mechanism which prevents proviral DNA integration into the CD4+ cell chromosome. Promising results have been seen in clinical trials in treatment-naïve and -experienced infected individuals. CCR5 antagonists bind to CCR5, one of the second receptors of HIV-1, and inhibit HIV-1 entry into CD4+ cells ...
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