Saquinavir half life
If you are taking birth control pills, saquinavir may decrease the effectiveness of the pills.
PfPM-IV have significant changes in polarity in the S3 and S3 pockets caused by the alterations of Thr 114 in PfPM-II to Ile in PfPM-IV at the S3 pocket and the contributions of Met 75 and Asn 76 PfPM-II ; compared to Ser and Ile in PfPM-IV at S3 . The S2 and S1 subsites are also smaller in PfPM-II than in PfPM-IV. The difference in the S2 subsite is due to the substitution of Leu 292 in PfPM-II for Val in PfPM-IV, and the change in the S1 pocket is due to the substitution of Phe at residue 111 PfPM-II ; for Leu in PfPM-IV. Changes are also found in the S1 subsite as the replacement of Phe 294 and Val 78 with Ile and Gly, respectively, in PfPM-IV results in this pocket being smaller in PfPM-II than in PfPM-IV. These variations suggest that PfPM-II has smaller subsites and is more limiting in its capacity to accommodate ligands with bulky substituents, and this can be seen experimentally using synthetic inhibitors 61 ; . Ligand docking studies below have focused principally on the active sites of PfPM-II and PfPM-IV, for which there are crystal structures. Comparison between ligand conformations bound to plasmepsin II and those bound to HIV-1 protease. Before docking HIV protease inhibitors into plasmepsins, we compared and analyzed known crystal structures of the HIV-1 protease in complex with the ligands in Table 1 and compared them with crystal structures of PfPM-II in complex with known ligands Fig. 5 ; . In each case there was high conservation of an extended beta-strand conformation for ligand backbones RMSD, 0.78 and 0.39 , respectively ; and highly conserved ligand side chain locations. This striking superimposition of these two sets of protease-bound ligand conformations Fig. 5, bottom ; reveals high similarity in the aspartyl protease binding of the ligands and supports the idea that HIV-1 protease ligands may have affinity for PfPM-II. Inhibition of PfPM-II and PfPM-IV enzymes. To validate the hypothesis that plasmepsins may be targets of the ARPIs, three inhibitors saquinavir, ritonavir, and lopinavir ; were assayed against recombinant PfPM-II and PfPM-IV enzymes Table 3 ; . Only one compound saquinavir ; showed submicromolar inhibitory potency against PfPM-II and PfPM-IV. The other two compounds had low and similar IC50 values, reflecting their similar structures. All of their IC50 concentrations are below the levels achieved in individuals treated with these drugs for HIV infection Table 1 ; , suggesting that they would be active at the concentrations reached in vivo during antiretroviral therapy. Docking of HIV protease inhibitors in P. falciparum plasmepsins II and IV. Initial validation of the ligand docking protocol was first performed using the GOLD program ; on the known PfPM-II inhibitor EH58 PDB code 1lf3 ; into PfPM-II and pepstatin A into PfPM-IV PDB code 1ls5 ; . Docking results were compared with the crystal structures and agreed best PfPM-II: RMSD, 0.63; PfPM-IV: RMSD, 0.73 ; when the modeling protocol incorporating all three PfPM-II ; or two PfPM-IV ; H-bond restraints was used. Using this validated modeling protocol, the three HIV protease inhibitors for which we have plasmepsin inhibition data were docked into PfPM-II and PfPM-IV. Docked structures for saquinavir, ritonavir Fig. 6 ; , and lopinavir were analyzed for hydrogen bonding interactions, interaction energies, and hydrophobic contacts using Ludi. The structural results suggest that the hydrophobic and hydrogen bonding interactions be.
Saquinavir order
The HIV-1 protease inhibitor, saquinavir SQV ; , 1 was the first of a new class of agents for the treatment of HIV disease and is a highly selective inhibitor of the HIV protease enzyme Kitchen et al., 1995; Schapiro et al., 1996 ; . When administered alone or in combination with reverse transcriptase inhibitors, a significant decrease in viral load is observed Collier et al., 1996 ; . However, the hard gelatin capsule formulation of SQV, Invirase, exhibits low oral bioavailability, measured as 4% in healthy volunteers after a single dose and estimated to be approximately 10% at steady state in HIV-positive patients Noble and Faulds, 1996; Perry and Noble, 1998 ; . To increase drug exposure, a new soft gel formulation of SQV, Fortovase, has been introduced with a bioavailability approximately three times that of Invirase. SQV is highly protein-bound 97% ; Halifax et al., 1998 ; . Although SQV has been shown to significantly reduce viral loads in patients, treatment failures and the emergence of resistance are probThis work was supported in part by National Institutes of Health, U.S. Public Health Service Training Grant GM07065 to T.F.B. ; and a Postdoctoral Fellowship from Merck-UNCF to C.B.W. ; . 1 Abbreviations used are: SQV, saquinavir; P-gp, P-glycoprotein; AUC, Area under the time versus concentration curve; CSF, cerebrospinal fluid; CNS, central nervous system. Send reprint requests to: Dr. Terrence F. Blaschke, Division of Clinical Pharmacology, S-009 Stanford University Medical Center, Stanford, CA 943055130. E-mail: blaschke stanford!
DFCI indicates Dana-Farber Cancer Institute; BWH, Brigham and Women's Hospital; MINN, University of Minnesota; OHSU, Oregon Health and Science University; and RPCI, Roswell Park Cancer Institute. * Unknown values were not used in the calculation of the P values. Good risk indicates CML in first chronic phase CP1 ; , acute myeloid leukemia AML ; and acute lymphoblastic leukemia ALL ; in complete response 1 CR1 ; , aplastic anemia. Intermediate risk indicates CML in accelerated phase AP AML and ALL in CR2 or above; non-Hodgkin lymphoma NHL ; , multiple myeloma MM ; , Hodgkin disease HD ; in partial response PR plus everyone else not good or poor. Poor risk indicates refractory or relapsed disease.
Downloaded from aac.asm by on March 13, 2008 FIG. 5. Inhibition of saquinavir 3 M ; efflux following equilibration with MK-571 and GF120918 1 M ; on both surfaces of MDCKII wt A ; , MDCKII-MRP1 B ; , and MDCKII-MRP2 C ; cell monolayers. AP3BL and BL3AP permeabilities are designated. Each data point represents the mean standard deviation n 4 ; . The following significant differences are indicated: a, the efflux ratio for 0 M MK-571 35 and 75 M MK-571 P 0.05 b, the efflux ratio for 0 M MK-571 35 and 75 M MK-571 P 0.05 c, the efflux ratio for 0 M MK-571 35 and 75 M MK-571 P 0.05 d, the efflux ratio for 35 M MK-571 75 M MK-571 P 0.05.
In addition, concomitant administration of sporanox ® and indinavir and ritonavir but not saquinavir ; may increase plasma concentrations of itraconazole and scopolamine.
Saquinavir half life
Roche has presented data suggesting that hiv that is resistant to saquinavir remains susceptible to other protease inhibitors, but other researchers, including scientists at merck, remain concerned that cross-resistance could occur.
In vitro studies: Sildenafil is a weak inhibitor of the cytochrome P450 isoforms 1A2, 2C9, 2C19, and 3A4 IC50 150 M ; . In vivo studies: When sildenafil 100 mg oral was co-administered with amlodipine, 5 mg or 10 mg oral, to hypertensive patients, the mean additional reduction on supine blood pressure was 8 mmHg systolic and 7 mmHg diastolic. No significant interactions were shown with tolbutamide 250 mg ; or warfarin 40 mg ; , both of which are metabolized by CYP2C9. Sildenafil 50 mg ; did not potentiate the increase in bleeding time caused by aspirin 150 mg ; . Sildenafil 50 mg ; did not potentiate the hypotensive effect of alcohol in healthy volunteers with mean maximum blood alcohol levels of 0.08%. Sildenafil at steady state 80 mg t.i.d. ; resulted in a 50% increase in AUC and a 42% increase in Cmax of bosentan 125 mg b.i.d. ; . In a study of healthy volunteers, sildenafil 100 mg ; did not affect the steady-state pharmacokinetics of the HIV protease inhibitors saquinavir and ritonavir, both of which are CYP3A4 substrates. Sildenafil had no impact on the plasma levels of oral contraceptives ethinyl estradiol 30 g and levonorgestrel 150 g ; . Carcinogenesis, Mutagenesis, Impairment of Fertility Sildenafil was not carcinogenic when administered to rats for up to 24 months at 60 mg kg day, a dose resulting in total systemic exposure AUC ; to unbound sildenafil and its major metabolite 33 and 37 times, for male and female rats, respectively, the human exposure at the Recommended Human Dose RHD ; of 20 mg t.i.d. Sildenafil was not carcinogenic when administered to male and female mice for up to 21 and 18 months, respectively, at doses up to a maximally tolerated level of 10 mg kg day, a dose equivalent to the RHD on a mg m2 basis. Sildenafil was negative in in vitro bacterial and Chinese hamster ovary cell assays to detect mutagenicity, and in vitro human lymphocyte and in vitro mouse micronucleus assays to detect clastogenicity. There was no impairment of fertility in male or female rats given up to 60 mg sildenafil kg day, a dose producing a total systemic exposure AUC ; to unbound sildenafil and its major metabolite 19 and 38 times, for males and females, respectively, the human exposure at the RHD of 20 mg t.i.d. Pregnancy Pregnancy Category B. No evidence of teratogenicity, embryotoxicity or fetotoxicity was observed in pregnant rats or rabbits, dosed with 200 mg sildenafil kg day during organogenesis, a level that is, on a mg m2 basis, 32- and 68-times, respectively, the RHD of 20 mg t.i.d. In a rat pre- and postnatal development study, the no-observed-adverse-effect dose was 30 mg kg day equivalent to 5-times the RHD on a mg m2 basis ; . There are no adequate and well-controlled studies of sildenafil in pregnant women. Nursing Mothers It is not known if sildenafil citrate and or metabolites are excreted in human breast milk. Since many drugs are excreted in human milk, caution should be used when REVATIO is administered to nursing women. Pediatric Use Safety and Effectiveness of sildenafil in pediatric pulmonary hypertension patients has not been established. Geriatric Use Healthy elderly volunteers 65 years or over ; had a reduced clearance of sildenafil, but studies did not include sufficient numbers of subjects to determine whether they respond differently from younger subjects. Other reported clinical experience has not identified differences in response between the elderly and younger pulmonary arterial hypertension patients. In general, dose selection for an elderly patient should be cautious, reflecting the greater frequency of decreased hepatic, renal, or cardiac function, and of concomitant disease or other drug therapy. ADVERSE REACTIONS Safety data were obtained from the pivotal study and an open-label extension study in 277 treated patients with pulmonary arterial hypertension. Doses up to 80 mg t.i.d. were studied. The overall frequency of discontinuation in REVATIO-treated patients at the recommended dose of 20 mg t.i.d. was low 3% ; and the same as placebo 3% ; . In the pivotal placebo-controlled trial in pulmonary arterial hypertension, the adverse drug reactions that were reported by at least 3% of REVATIO patients treated at the recommended dosage 20 mg t.i.d. ; and were more frequent in REVATIO patients than placebo patients, are shown in Table 2. Adverse events were generally transient and mild to moderate in nature. TABLE 2. Sildenafil Adverse Events in 3% of Patients and More Frequent Than Placebo and secobarbital.
Saquinavir dosage
Acknowledgements We would like to thank Burroughs Wellcome Inc., for supporting this study. The following were also instrumental in providing technical and administrative assistance: Shelagh Benning, Knut Borkenhagen, Jeanine Robinson and Christine Rachue. References Berning, S. E., Huitt, G. A., Iseman, M. D. & Peloquin, C. A. 1992 ; . Letter to the editor: Malabsorption of antituberculous medications by a patient with AIDS. New England Journal of Medicine 327, 1817-8. Burger, D. M., Meenhorst, P. L., ten Napel, C. H. H., Mulder, J. W., Neef, C , Koks, C. H. W. et al. 1994 ; . Pharmacokinetic variability of zidovudine in HIV-infected individuals: subgroup analysis and drug interactions. AIDS 8, 1683-9. Escolano, S., Mentre, F., Golmard, J. L., Diquet, B. & Mallet, A. 1991 ; . Letter to the editor. New England Journal of Medicine 324, 995. Fischl, M. A., Parker, C. B., Pettinelli, C , Wulfsohn, M., Hirsch, M. S., Collier, A. C. et al. 1990 ; . A randomized controlled trial of a reduced daily dose of zidovudine in patients with the acquired immunodeficiency syndrome. New England Journal of Medicine 323, 1009--14. Hu, M. 1993 ; . Comparison of uptake characteristics of thymidine and zidovudine in a human intestinal epithelial model system. Journal of Pharmaceutical Sciences 82, 829-33. Kapembwa, M. S., Fleming, S. C , Sewankambo, N., Serwadda, D., Lucas, S., Moody, A. et al. 1991 ; . Altered small-intestinal permeability associated with diarrhoea in Caucasian and African subjects. Clinical Science 81, 327-34. Macnab, K. A., Gill, M. J., Sutherland, L. R., De Boer Visser, N. & Church, D. 1993 ; . Erratic zidovudine bioavailability in HIV seropositive patients. Journal of Antimicrobial Chemotherapy 31, 421-8. Sahai, J., Gallicano, K., Ormsby, E., Garber, G. & Cameron, D. W. 1994 ; . Relationship between body weight, body surface area and serum zidovudine pharmacokinetic parameters in adult, male HIV-infected patients. AIDS 8, 793-6. Sale, M., Sheiner, L. B., Volberding, P. & Blaschke, T. F. 1993 ; . Zidovudine response relationships in early human immunodeficiency virus infection. Clinical Pharmacology and Therapeutics 54, 556-66. Wilde, M. I. & Langtry, H. D. 1993 ; . Zidovudine. And update of its pharmacodynamic and pharmacokinetic properties, and therapeutic efficacy. Drugs 46, 515-78. Received 3 July 1995; returned 2 August 1995; revised 3 October 1995; accepted 21 November 1995.
All recombinant viral clones containing the I50L substitution in a variety of genetic backgrounds. Recombinant viruses containing either I50L or I50L A71V were growth impaired and showed increased susceptibility to all of the other PIs tested. Lastly, there was no evidence of crossresistance between atazanavir and amprenavir, with insertion of the I50L and I50V substitutions yielding selective resistance to atazanavir and amprenavir, respectively. Treatment Naive Patients: Phenotypic and genotypic analyses from patients experiencing virologic failure while on REYATAZ confirmed that the I50L substitution resulted in decreased susceptibility to atazanavir. All 23 resistant isolates from studies in treatment-naive patients had an I50L substitution that emerged on REYATAZ therapy. Apart from the A71V substitution, which is commonly observed in many protease inhibitor resistance pathways, none of the other amino acid changes observed appeared to correlate with atazanavir resistance. Resistance levels to atazanavir ranged from 3.5 to 29-fold. Treatment -Experienced patients: Among the 42 isolates from treatment-experienced patients who developed resistance to atazanavir on therapy that included REYATAZ or REYATAZ ritonavir, 9 isolates displayed the I50L substitution. The remaining 33 isolates showed no evidence of the I50L substitution and no obvious pattern of change beyond the accumulation of primary and secondary resistance substitutions involved in PI resistance. These isolates developed higher levels of resistance to other PIs as well as REYATAZ. The 32 resistant isolates from treatment-experienced patients who were treated with the PI combination of REYATAZ saquinavir showed no obvious pattern of changes beyond the accumulation of the primary and secondary resistance substitutions involved in PI resistance. Isolates resistant to REYATAZ from PI-experienced patients were also cross resistant to other PIs. There was no indication that any of these isolates developed the I50L substitution. Cross-resistance: Cross resistance among PIs has been observed. Baseline phenotypic and genotypic analyses of clinical isolates from REYATAZ clinical trials of PI-experienced patients showed that isolates cross-resistant to multiple PIs were cross-resistant to REYATAZ. Isolates resistant to REYATAZ were also cross resistant to other PIs. An association between virologic response of 48 weeks and the number of primary PI-resistance-associated substitutions detected in baseline HIV-1 isolates from antiretroviral-experienced patients in Study AI424-045 Table 17 ; significantly favoured the lopinavir ritonavir arm when considering patients with 4 or more PI substitutions. Genotypic and or phenotypic analysis of baseline virus may aid in determining ATV susceptibility before initiation of REYATAZ ritonavir therapy and senna.
Saquinavir cream
Once-daily dosing of saquinavir with ritonavir is being studied.
[79] Burger DM, Bergshoeff AS, De Groot R, Gibb D, Walker S, Treluyer JM, et al. Maintaining the nelfinavir trough concentration above 0.8 mg L improves virologic response in HIV-1-infected children. J Pediatr. 2004 Sep; 145 3 ; : 403-5. [80] Floren LC, Wiznia A, Hayashi S, Jayewardene A, Stanley K, Johnson G, et al. Nelfinavir pharmacokinetics in stable human immunodeficiency virus-positive children: Pediatric AIDS Clinical Trials Group Protocol 377. Pediatrics. 2003 Sep; 112 3 Pt 1 ; e220-7. [81] King JR, Nachman S, Yogev R, Hodge J, Aldrovandi G, Hughes MD, et al. Efficacy, tolerability and pharmacokinetics of two nelfinavir-based regimens in human immunodeficiency virus-infected children and adolescents: pediatric AIDS clinical trials group protocol 403. Pediatr Infect Dis J. 2005 Oct; 24 10 ; : 880-5. [82] Schuster T, Linde R, Wintergerst U, Funk MB, Kurowski M, Kreuz W, et al. Nelfinavir pharmacokinetics in HIV-infected children: a comparison of twice daily and three times daily dosing. Aids. 2000 Jul 7; 14 10 ; : 1466-8. [83] Krogstad P, Wiznia A, Luzuriaga K, Dankner W, Nielsen K, Gersten M, et al. Treatment of human immunodeficiency virus 1-infected infants and children with the protease inhibitor nelfinavir mesylate. Clin Infect Dis. 1999 May; 28 5 ; : 1109-18. [84] Hoffmann F, Notheis G, Wintergerst U, Eberle J, Gurtler L, Belohradsky BH. Comparison of ritonavir plus saquinavir- and nelfinavir plus saquinavir-containing regimens as salvage therapy in children with human immunodeficiency type 1 infection. Pediatr Infect Dis J. 2000 Jan; 19 1 ; : 47-51. [85] Grub S, Schwarzwald HL, Kline MW, Jorga K. Pharmacokinetics of saquinavir in children during long term treatment. Pediatr Infect Dis J. 2002 Jul; 21 7 ; : 712-3. [86] Kline MW, Brundage RC, Fletcher CV, Schwarzwald H, Calles NR, Buss NE, et al. Combination therapy with saquinavir soft gelatin capsules in children with human immunodeficiency virus infection. Pediatr Infect Dis J. 2001 Jul; 20 7 ; : 666-71. [87] Bergshoeff AS, Fraaij PL, van Rossum AM, Wolfs TF, Geelen SP, de Groot R, et al. Pharmacokinetics of nelfinavir in children: influencing factors and dose implications. Antivir Ther. 2003 Jun; 8 3 ; : 215-22. [88] Hoffmann F, Funk M, Linde R, Notheis G, Petropoulou T, Eberle J, et al. Effect of antiretroviral triple combinations including the protease inhibitor nelfinavir in heavily pretreated children with HIV-1 infection. Eur J Med Res. 2002 Jul 24; 7 ; : 330-4. [89] Crommentuyn KM, Scherpbier HJ, Kuijpers TW, Mathot RA, Huitema AD, Beijnen JH. Population pharmacokinetics and pharmacodynamics of nelfinavir and its active metabolite M8 in HIV-1-infected children. Pediatr Infect Dis J. 2006 Jun; 25 6 ; : 538-43. [90] Hirt D, Urien S, Jullien V, Firtion G, Rey E, Pons G, et al. Age-related effects on nelfinavir and M8 pharmacokinetics: a population study with 182 children. Antimicrob Agents Chemother. 2006 Mar; 50 3 ; : 910-6. [91] van Heeswijk RP, Scherpbier HJ, de Koning LA, Heymans HS, Lange JM, Beijnen JH, et al. The pharmacokinetics of nelfinavir in HIV-1-infected children. Ther Drug Monit. 2002 Aug; 24 4 ; : 487-91. [92] Gatti G, Castelli-Gattinara G, Cruciani M, Bernardi S, De Pascalis CR, Pontali E, et al. Pharmacokinetics and pharmacodynamics of nelfinavir administered twice or thrice daily to human immunodeficiency virus type 1-infected children. Clin Infect Dis. 2003 Jun 1; 36 11 ; : 1476-82. [93] Grub S, Delora P, Ludin E, Duff F, Fletcher CV, Brundage RC, et al. Pharmacokinetics and pharmacodynamics of saquinavir in pediatric patients with human immunodeficiency virus infection. Clin Pharmacol Ther. 2002 Mar; 71 3 ; : 122-30. [94] Ananworanich J, Kosalaraksa P, Hill A, Siangphoe U, Bergshoeff A, Pancharoen C, et al. Pharmacokinetics and 24-week efficacy safety of dual boosted saquinavir lopinavir ritonavir in nucleoside-pretreated children. Pediatr Infect Dis J. 2005 Oct; 24 10 ; : 874-9 and septra.
Saquinavir dosage
Plication fee ; from the U.S. Government in exchange for developing a therapy for a rare disease or condition, defined as a disease that affects fewer than 200, 000 individuals in this country. The drug must then go through the FDA marketing approval process like any other drug or biologic, but the process is often expedited. To date over 1400 drugs and biologics have been designated as orphan-drugs, and over 250 have been approved for marketing since the Office of Orphan Products Development began in 1983. Because the cost of developing drugs is so high, such small markets would rarely be targeted for drug development without this help Overall response rate: the proportion of patients who have a response to the treatment, as defined by the study protocol; usually means the sum of complete and partial responses, but some studies also include minor responses. In cancer treatment, response is defined as shrinkage of the tumor. A partial response is often defined as tumor shrinkage of 50% or more. Oxidative stress: the collective term used to describe the formation of toxic free radicals and other reactive oxygen species ROS ; and their deleterious effect on cell function See Appendix I P: See Statistical significance. Palliation: mitigation; reduction in the severity. Palliative chemotherapy is given in advanced disease when a cure cannot be expected but shrinkage of the tumor will provide some relief from pain and discomfort.
Based upon pharmacokinetic data and moderate experience with use in pregnancy, ritonavirboosted saquinavir can be considered a preferred PI for combination regimens in pregnancy.2 * -- 2005 Recommendations for Use of Antiretroviral Drugs in Pregnant HIV-1-Infected Women for Maternal Health Tolerability and safety of INVIRASE and serostim.
Drugs 2000; 59: 58162 antivirals primarily j05 , also s01ad and d06bb ; anti- herpesvirus aciclovir cidofovir docosanol famciclovir fomivirsen foscarnet ganciclovir idoxuridine penciclovir trifluridine tromantadine valaciclovir valganciclovir vidarabine anti- influenza agents arbidol adamantane derivatives m2 inhibitors amantadine , rimantadine ; neuraminidase inhibitors oseltamivir , peramivir , zanamivir ; antiretrovirals : nrtis abacavir didanosine emtricitabine lamivudine stavudine zalcitabine zidovudine antiretrovirals: ntrtis adefovir tenofovir antiretrovirals: nnrtis antiretrovirals: pis amprenavir atazanavir darunavir fosamprenavir indinavir lopinavir nelfinavir ritonavir saquinavir tipranavir antiretrovirals: fusion inhibitors antiretrovirals: integrase inhibitors other antiviral agents general inosine , interferon ; hiv maraviroc ; picornavirus pleconaril ; human papillomavirus molluscum contagiosum imiquimod , podophyllotoxin ; hepatitis c ribavirin , viramidine ; this entry is from wikipedia, the leading user-contributed encyclopedia.
| Saquinavir approvalResearchers at several sites in the U.S. recruited 21 HIV positive subjects for this study which compared the effect of two different boosted protease inhibitor PI ; regimens: saquinavir Fortovase ; 400 mg with ritonavir Norvir ; 400 mg, both twice daily saquinavir 1, 000 mg with ritonavir 100 mg, both twice daily The PI combinations were taken with two or and sevelamer.
Saquinavir level
ANTIRETROVIRALS NRTIs- abacavir Ziagen ; , abacavir lamivudine Epzicom ; , abacavir lamivudine zidovudine Trizivir ; , didanosine ddI, Videx, Videx EC ; , emtricitabine Emtriva ; , lamivudine Epivir, 3TC ; , lamivudine zidovudine Combivir ; , stavudine d4T, Zerit ; , tenofovir Viread ; , tenofovir emtricitabine Truvada ; , zalcitabine ddC, Hivid ; , zidovudine AZT, Retrovir ; . PIs- amprenavir Agenerase ; , atazanavir Reyataz ; , fos-amprenavir calcium Lexiva ; , indinavir Crixivan ; , lopinavir ritonavir Kaletra ; , nelfinavir Viracept ; , ritonavir Norvir ; , saquinavir Fortovase, Invirase ; , tipranavir Aptivus ; . NNRTIs- delavirdine Rescriptor ; , efavirenz Sustiva ; , nevirapine Viramune ; . Otherhydroxyurea Hydrea ; . Entry Inhibitors- enfuvirtide Fuzeon ; . OI DRUGS PHS "A1 OI"s- acyclovir Zovirax ; , amphotericin B, azithromycin Zithromax ; , cidofovir Vistide ; , clarithromycin Biaxin ; , clindamycin, famciclovir Famvir ; , fluconazole Diflucan ; , flucytosine, fomivirsen, foscarnet Foscavir ; , ganciclovir Cytovene ; , isoniazid INH ; , itraconazole Sporonox ; , leucovorin, peg-interferon alfa-2b * , pentamidine, pentavalent antimony, prednisone, probenecid, pyrazinamide, pyrimethamine Daraprim, Fansidar ; , ribavirin * , rifabutin, rifampin, sulfadiazine, TMP SMX Bactrim ; , valacyclovir, valganciclovir. ALL OTHERS Open Formulary - All FDA approved drugs are covered except the following: Specific open formulary exclusions: antirheumatic injectables e.g. Enbrel ; , botulinum toxin e.g. botox, mylobloc ; compounded medications for infusion active medication containing more than one ingredient ; , gonadotropin, finasteride Propecia ; , hyaluronic acid derivatives e.g. Hyalgan, Synvisc ; , immune globulin intravenous IGIV e.g. sandoglobulin, Venoglobulin ; , injectable muscle relaxants e.g. Lioresal ; , mifepristone, minoxidil Rogaine ; , monoclonal antibodies e.g. Remicade, Synagis ; , propoxyphene, recombinant human growth hormone HGH e.g. Geref, Humatrop ; , Viagra. Class Exclusions: cosmetic medications, durable medical equipment, erectile dysfunction pharamaceuticals, fertility drugs, herbal medications, immunizing biologicals, nutritional supplements and saquinavir.
1. 2. 3. Lesser PF. Florida grapefruit-juice developments. Presented at: FoodNews Second International Fruit-Juice Conference; October 7, 1997; Amsterdam, the Netherlands. Cerda JJ, Normann SJ, Sullivan MP, et al. Inhibition of atherosclerosis by dietary pectin in microswine with sustained hypercholesterolemia. Circulation. 1994; 89: 1247-1253. So FV, Guthrie N, Chambers AF, Moussa M, Carroll KK. Inhibition of human breast cancer cell proliferation and delay of mammary tumorigenesis by flavonoids and citrus juices. Nutr Cancer. 1996; 26: 167-181. Guthrie N, Carroll KK. Inhibition of mammary cancer by citrus flavonoids. Adv Exp Med Biol. 1998; 439: 227-236. Bailey DG, Spence JD, Edgar B, Bayliff CD, Arnold JM. Ethanol enhances the hemodynamic effects of felodipine. Clin Invest Med. 1989; 12: 357-362. Bailey DG, Spence JD, Munoz C, Arnold JM. Interaction of citrus juices with felodipine and nifedipine. Lancet. 1991; 337: 268-269. Edgar B, Bailey D, Bergstrand R, Johnsson G, Regardh CG. Acute effects of drinking grapefruit juice on the pharmacokinetics and dynamics of felodipine--and its potential clinical relevance. Eur J Clin Pharmacol. 1992; 42: 313-317. Zhang QY, Dunbar D, Ostrowska A, Zeisloft S, Yang J, Kaminsky LS. Characterization of human small intestinal cytochromes P-450. Drug Metab Dispos. 1999; 27: 804-809. Kivisto KT, Lamberg TS, Kantola T, Neuvonen PJ. Plasma buspirone concentrations are greatly increased by erythromycin and itraconazole. Clin Pharmacol Ther. 1997; 62: 348-354. Kivisto KT, Kantola T, Neuvonen PJ. Different effects of itraconazole on the pharmacokinetics of fluvastatin and lovastatin. Br J Clin Pharmacol. 1998; 46: 49-53. Floren LC, Bekersky I, Benet LZ, et al. Tacrolimus oral bioavailability doubles with coadministration of ketoconazole. Clin Pharmacol Ther. 1997; 62: 41-49. Azie NE, Brater DC, Becker PA, Jones DR, Hall SD. The interaction of diltiazem with lovastatin and pravastatin. Clin Pharmacol Ther. 1998; 64: 369-377. Lundahl J, Regardh CG, Edgar B, Johnsson G. Effects of grapefruit juice ingestion--pharmacokinetics and haemodynamics of intravenously and orally administered felodipine in healthy men. Eur J Clin Pharmacol. 1997; 52: 139-145. Rashid TJ, Martin U, Clarke H, Waller DG, Renwick AG, George CF. Factors affecting the absolute bioavailability of nifedipine. Br J Clin Pharmacol. 1995; 40: 51-58. Kupferschmidt HH, Fattinger KE, Ha HR, Follath F, Krahenbuhl S. Grapefruit juice enhances the bioavailability of the HIV protease inhibitor saquinavir in man. Br J Clin Pharmacol. 1998; 45: 355359. Kupferschmidt HH, Ha HR, Ziegler WH, Meier PJ, Krahenbuhl S. Interaction between grapefruit juice and midazolam in humans. Clin Pharmacol Ther. 1995; 58: 20-28. Hostetler KA, Wrighton SA, Molowa DT, Thomas PE, Levin W, Guzelian PS. Coinduction of multiple hepatic cytochrome P-450 proteins and their mRNAs in rats treated with imidazole antimycotic agents. Mol Pharmacol. 1989; 35: 279-285. Lown KS, Bailey DG, Fontana RJ, et al. Grapefruit juice increases felodipine oral availability in humans by decreasing intestinal CYP3A protein expression. J Clin Invest. 1997; 99: 2545-2553 and sirolimus.
Saquinavir brand name
| Electron Microscopic Study of the Experimental Myelogenous Leukemia Li-Tsun Chen, Evelyn E. Handler, Eugene.
Saquinavir pharmacokinetics
Obsessive compulsive disorder tips, sedimentation rate 38, lymphoid throat mass, nefazodone availability and herbalism gold. Zocor cholesterol medicine, tagged red blood cell scan, alternate nostril breathing and emotional quotient by goleman or humalog 17 units.
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