Sexually Transmitted Diseases in Women (STDs) »
Sexually transmitted diseases (STDs) are infections that can be transferred from one person to another through any type of sexual contact. STDs are sometimes referred to as sexually transmitted infections (STIs) since they involve the transmission of a disease-causing organism from one person to another during sexual activity. It is important to realize that sexual contact includes more than just sexual intercourse (vaginal and anal). Sexual contact includes kissing, oral-genital contact, and the use of sexual "toys," such as vibrators. STDs probably have been around for thousands of years, but the most dangerous of these conditions, the acquired immunodeficiency syndrome (AIDS or HIV disease), has only been recognized since 1984.
Many STDs are treatable, but effective cures are lacking for others, such as HIV, HPV, and hepatitis B and hepatitis C. Even gonorrhea, once easily cured, has become...
Read the Sexually Transmitted Diseases in Women (STDs) article »
|
|
Adefovir is an antiviral drug.
The pharmacokinetics of adefovir have been evaluated in healthy volunteers and patients with chronic hepatitis B. Adefovir pharmacokinetics are similar between these populations.
Adefovir dipivoxil is a diester prodrug of the active moiety adefovir. Based on a cross study comparison, the approximate oral bioavailability of adefovir from HEPSERA (adefovir dipivoxil) is 59%.
Following oral administration of a 10 mg single dose of HEPSERA (adefovir dipivoxil) to chronic hepatitis B patients (N=14), the peak adefovir plasma concentration (Cmax) was 18.4 ± 6.26 ng/mL (mean ± SD) and occurred between 0.58 and 4.00 hours (median=1.75 hours) post dose. The adefovir area under the plasma concentration-time curve (AUC0-∞) was 220 ± 70.0 ng•h/mL. Plasma adefovir concentrations declined in a biexponential manner with a terminal elimination half-life of 7.48 ± 1.65 hours.
The pharmacokinetics of adefovir in subjects with adequate renal function were not affected by once daily dosing of 10 mg HEPSERA (adefovir dipivoxil) over seven days. The impact of long-term once daily administration of 10 mg HEPSERA (adefovir dipivoxil) on adefovir pharmacokinetics has not been evaluated.
Adefovir exposure was unaffected when a 10 mg single dose of HEPSERA (adefovir dipivoxil) was administered with food (an approximately 1000 kcal high-fat meal). HEPSERA (adefovir dipivoxil) may be taken without regard to food.
In vitro binding of adefovir to human plasma or human serum proteins is ≤ 4% over the adefovir concentration range of 0.1 to 25 µg/mL. The volume of distribution at steady-state following intravenous administration of 1.0 or 3.0 mg/kg/day is 392 ± 75 and 352 ± 9 mL/kg, respectively.
Following oral administration, adefovir dipivoxil is rapidly converted to adefovir. Forty-five percent of the dose is recovered as adefovir in the urine over 24 hours at steady state following 10 mg oral doses of HEPSERA (adefovir dipivoxil) . Adefovir is renally excreted by a combination of glomerular filtration and active tubular secretion [see DRUG INTERACTIONS].
Adefovir dipivoxil is rapidly converted to adefovir in vivo. At concentrations substantially higher ( > 4000-fold) than those observed in vivo, adefovir did not inhibit any of the common human CYP450 enzymes, CYP1A2, CYP2C9, CYP2C19, CYP2D6, and CYP3A4. Adefovir is not a substrate for these enzymes. However, the potential for adefovir to induce CYP450 enzymes is unknown. Based on the results of these in vitro experiments and the renal elimination pathway of adefovir, the potential for CYP450 mediated interactions involving adefovir as an inhibitor or substrate with other medicinal products is low.
The pharmacokinetics of adefovir have been evaluated in healthy adult volunteers following multiple dose administration of HEPSERA (adefovir dipivoxil) (10 mg once daily) in combination with lamivudine (100 mg once daily) (N=18), trimethoprim/sulfamethoxazole (160/800 mg twice daily) (N=18), acetaminophen (1000 mg four times daily) (N=20), ibuprofen (800 mg three times daily) (N=18), and enteric coated didanosine (400 mg) (N=21). The pharmacokinetics of adefovir have also been evaluated in post-liver transplantation patients following multiple dose administration of HEPSERA (adefovir dipivoxil) (10 mg once daily) in combination with tacrolimus (N=16). The pharmacokinetics of adefovir have been evaluated in healthy volunteers following single dose pegylated interferon α-2a (PEG-IFN) (180 µg) (N=15).
Adefovir did not alter the pharmacokinetics of lamivudine, trimethoprim/sulfamethoxazole, acetaminophen, ibuprofen, enteric coated didanosine (didanosine EC), or tacrolimus. The evaluation of the effect of adefovir on the pharmacokinetics of pegylated interferon α-2a was inconclusive due to the high variability of pegylated interferon alpha-2a.
The pharmacokinetics of adefovir were unchanged when HEPSERA (adefovir dipivoxil) was coadministered with lamivudine, trimethoprim/sulfamethoxazole, acetaminophen, didanosine EC, tacrolimus (based on cross study comparison), and pegylated interferon α-2a. When HEPSERA (adefovir dipivoxil) was coadministered with ibuprofen (800 mg three times daily) increases in adefovir Cmax (33%), AUC (23%) and urinary recovery were observed. This increase appears to be due to higher oral bioavailability, not a reduction in renal clearance of adefovir.
Apart from lamivudine, trimethoprim/sulfamethoxazole, and acetaminophen, the effects of co-administration of HEPSERA (adefovir dipivoxil) with drugs that are excreted renally, or other drugs known to affect renal function have not been evaluated.
The effect of adefovir on cyclosporine concentrations is not known.
No drug interaction studies have been performed in adolescent patients aged ≥ 12 years to < 18 years.
The pharmacokinetics of adefovir were similar in male and female patients.
The pharmacokinetics of adefovir have been shown to be comparable in Caucasians and Asians. Pharmacokinetic data are not available for other racial groups.
Pharmacokinetic studies have not been conducted in the elderly.
The pharmacokinetics of adefovir were assessed from drug plasma concentrations in 53 HBeAg positive hepatitis B pediatric patients with compensated liver disease. The exposure of adefovir following a 48 week daily treatment with adefovir dipivoxil 10 mg tablet in pediatric patients aged ≥ 12 to < 18 years (Cmax = 23.3 ng/ml and AUC0-24 = 248.8 ng•h/ml) was comparable to that observed in adult patients.
In adults with moderately or severely impaired renal function or with end-stage renal disease (ESRD) requiring hemodialysis, Cmax, AUC, and half-life (T1/2) were increased compared to adults with normal renal function. It is recommended that the dosing interval of HEPSERA be modified in these patients [see DOSAGE AND ADMINISTRATION].
The pharmacokinetics of adefovir in non-chronic hepatitis B patients with varying degrees of renal impairment are described in Table 3. In this study, subjects received a 10 mg single dose of HEPSERA (adefovir dipivoxil) .
Table 3: Pharmacokinetic Parameters (Mean ± SD) of
Adefovir in Patients with Varying Degrees of Renal Function
| Renal Function Group | Unimpaired | Mild | Moderate | Severe |
| Baseline creatinine clearance (mL/min) | > 80 (N=7) |
50–80 (N=8) |
30–49 (N=7) |
10–29 (N=10) |
| Cmax (ng/mL) | 17.8 ± 3.22 | 22.4 ± 4.04 | 28.5 ± 8.57 | 51.6 ± 10.3 |
| AUC 0-∞ (ng•h/mL) | 201 ± 40.8 | 266 ± 55.7 | 455 ± 176 | 1240 ± 629 |
| CL/F (mL/min) | 469 ± 99.0 | 356 ± 85.6 | 237 ± 118 | 91.7 ± 51.3 |
| CLrenal (mL/min) | 231 ± 48.9 | 148 ± 39.3 | 83.9 ± 27.5 | 37.0 ± 18.4 |
A four-hour period of hemodialysis removed approximately 35% of the adefovir dose. The effect of peritoneal dialysis on adefovir removal has not been evaluated.
The pharmacokinetics of adefovir have not been studied in adolescent patients with renal dysfunction [see Use in Specific Populations].
The pharmacokinetics of adefovir following a 10 mg single dose of HEPSERA (adefovir dipivoxil) have been studied in non-chronic hepatitis B patients with hepatic impairment. There were no substantial alterations in adefovir pharmacokinetics in patients with moderate and severe hepatic impairment compared to unimpaired patients. No change in HEPSERA (adefovir dipivoxil) dosing is required in patients with hepatic impairment.
Adefovir is an acyclic nucleotide analog of adenosine monophosphate which is phosphorylated to the active metabolite adefovir diphosphate by cellular kinases. Adefovir diphosphate inhibits HBV DNA polymerase (reverse transcriptase) by competing with the natural substrate deoxyadenosine triphosphate and by causing DNA chain termination after its incorporation into viral DNA. The inhibition constant (Ki) for adefovir diphosphate for HBV DNA polymerase was 0.1 µM. Adefovir diphosphate is a weak inhibitor of human DNA polymerases α and γ with Ki values of 1.18 µM and 0.97 µM, respectively.
The concentration of adefovir that inhibited 50% of viral DNA synthesis (EC50) in HBV transfected human hepatoma cell lines ranged from 0.2 to 2.5 µM. The combination of adefovir with lamivudine showed additive anti-HBV activity.
Clinical isolates with genotypic changes conferring reduced susceptibility in cell culture to nucleoside analog reverse transcriptase inhibitors for the treatment of HBV infection have been observed. Long-term resistance analyses performed by genotyping samples from all adefovir dipivoxil-treated patients with detectable serum HBV DNA demonstrated that amino acid substitutions rtN236T and rtA181T/V have been observed in association with adefovir resistance. In cell culture, the rtN236T substitution demonstrated 4- to 14-fold, the rtA181V substitution 2.5- to 4.2-fold, and the rtA181T substitution 1.3- to 1.9-fold reduced susceptibility to adefovir.
In HBeAg-positive nucleoside-naïve patient isolates (Study GS-98-437, N=171), no adefovir resistance-associated substitutions were observed at Week 48. Sixty-five patients continued on long term treatment after a median duration on adefovir dipivoxil of 235 weeks (range 110–279 weeks). Isolates from 16 of 38 (42%) patients developed adefovir resistance-associated substitutions in the setting of virologic failure (confirmed increase of ≥ 1 log10 HBV DNA copies/mL above nadir or never suppressed below 103 copies/mL). The substitutions included rtN236T (n=2), rtA181V (n=4), rtA181T (n=3), rtA181T+rtN236T (n=5), and rtA181V+rtN236T (n=2). In HBeAg-negative nucleoside-naïve patients (Study GS-98-438), isolates from 30 patients were identified with adefovir resistance-associated substitutions with a cumulative probability of 0%, 3%, 11%, 19%, and 30% at 48, 96, 144, 192, and 240 weeks, respectively. Of those 30 patients, 22 had a confirmed increase of ≥ 1 log10 HBV DNA copies/mL above nadir or never achieved HBV DNA levels below 103 copies/mL; an additional 8 patients had adefovir resistance-associated substitutions without virologic failure. In addition, the long term (4 to 5 years) development of resistance to adefovir dipivoxil was significantly lower in patients who had serum HBV DNA below the limit of quantification (less than 1,000 copies/mL) at Week 48 as compared to patients who had serum HBV DNA above 1,000 copies/mL at Week 48.
In an open-label study of pre- and post-liver transplantation patients (Study GS-98-435), isolates from 129 patients with clinical evidence of lamivudine-resistant hepatitis B virus at baseline were evaluated for adefovir resistance-associated substitutions. The incidence of adefovir resistance-associated (rtN236T or rtA181T/V) substitutions was 0% at 48 weeks. Isolates from four patients developed the rtN236T substitution after 72 weeks of adefovir dipivoxil therapy. Development of the rtN236T substitution was associated with serum HBV DNA rebound. All 4 patients who developed the rtN236T substitution in their HBV had discontinued lamivudine therapy before the development of genotypic resistance and all 4 lost the lamivudine resistance-associated substitutions present at baseline. In a study of 35 HIV/HBV co-infected patients with lamivudine-resistant HBV (Study 460i) who added adefovir dipivoxil to lamivudine, no adefovir resistance-associated substitutions were observed in HBV isolates from 15/35 patients tested up to 144 weeks of therapy.
Clinical resistance in pediatric patients
In a Phase 3 pediatric Study GS-US-103-518, HBV isolates from 49 of 56 pediatric subjects (aged 12 to 17 years) had serum HBV DNA > 169 copies/mL and were evaluated for adefovir resistance-associated substitutions. rtN236T and/or rtA181V adefovir resistance-associated substitutions were not observed at Week 48. However, the rtA181T substitution was present in baseline and Week 48 isolates from 2 pediatric patients.
Recombinant HBV variants containing lamivudine-resistance-associated substitutions (rtL180M, rtM204I, rtM204V, rtL180M + rtM204V, rtV173L + rtL180M + rtM204V) were susceptible to adefovir in cell culture. Adefovir dipivoxil has also demonstrated anti-HBV activity (median reduction in serum HBV DNA of 4.1 log10 copies/mL) in patients with HBV containing lamivudine-resistance-associated substitutions (Study 435). Adefovir also demonstrated in cell culture activity against HBV variants with entecavir resistance-associated substitutions (rtT184G, rtS202I, rtM250V). HBV variants with DNA polymerase substitutions rtT128N and rtR153Q or rtW153Q associated with resistance to hepatitis B virus immunoglobulin were susceptible to adefovir in cell culture.
HBV variants expressing the adefovir resistance-associated substitution rtN236T showed no change in susceptibility to entecavir in cell culture, and a 2- to 3-fold decrease in lamivudine susceptibility. HBV mutants with the adefovir resistance-associated substitution rtA181V showed a range of decreased susceptibilities to lamivudine of 1- to 14-fold and a 12-fold decrease in susceptibility to entecavir. In patients whose HBV expressed the rtA181V substitution (n=2) or the rtN236T substitution (n=3), a reduction in serum HBV DNA of 2.4 to 3.1 and 2.0 to 5.1 log10 copies/mL, respectively, was observed when treatment with lamivudine was added to treatment with adefovir dipivoxil.
Animal reproduction studies were conducted in rats and rabbits with orally administered adefovir dipivoxil and intravenously administered adefovir.
In rats and rabbits, no embryotoxicity or teratogenicity was shown from oral administration of adefovir dipivoxil at maternal doses producing systemic exposures approximately 23 times (rats) and 40 times (rabbits) that achieved in humans at the therapeutic dose of 10 mg/day.
When pregnant rats were administered intravenous adefovir at maternally toxic doses associated with systemic exposure 38 times that in humans, embryotoxicity and an increased incidence of fetal malformations (anasarca, depressed eye bulge, umbilical hernia, and kinked tail) were observed. No adverse effects on development were seen with intravenous adefovir administered to pregnant rats at a systemic exposure 12 times that in humans.
Renal tubular nephropathy characterized by histological alterations and/or increases in BUN and serum creatinine was the primary dose-limiting toxicity associated with administration of adefovir dipivoxil in animals. Nephrotoxicity was observed in animals at systemic exposures approximately 3–10 times higher than those in humans at the recommended therapeutic dose of 10 mg/day.
Study 437 was a randomized, double-blind, placebo-controlled, three-arm study in patients with HBeAg-positive chronic hepatitis B that allowed for a comparison between placebo and HEPSERA (adefovir dipivoxil) . The median age of patients was 33 years. Seventy-four percent were male, 59% were Asian, 36% were Caucasian, and 24% had prior interferon-α treatment. At baseline, patients had a median total Knodell Histology Activity Index (HAI) score of 10, a median serum HBV DNA level as measured by the Roche Amplicor Monitor polymerase chain reaction (PCR) assay (LLOQ = 1000 copies/mL) of 8.36 log10 copies/mL and a median ALT level of 2.3 times the upper limit of normal.
Study 438 was a randomized, double-blind, placebo-controlled study in patients who were HBeAg-negative at screening, and anti-HBe positive. The median age of patients was 46 years. Eighty-three percent were male, 66% were Caucasian, 30% were Asian and 41% had prior interferon-α treatment. At baseline, the median total Knodell HAI score was 10, the median serum HBV DNA level as measured by the Roche Amplicor Monitor PCR assay (LLOQ = 1000 copies/mL) was 7.08 log10 copies/mL, and the median ALT was 2.3 times the upper limit of normal.
The primary efficacy endpoint in both studies was histological improvement at Week 48; results of which are shown in Table 4.
Table 4: Histological Response at Week 48a
| Study 437 | Study 438 | |||
| HEPSERA (adefovir dipivoxil) 10 mg (N=168) |
Placebo (N=161) |
HEPSERA (adefovir dipivoxil) 10 mg (N=121) |
Placebo (N=57) |
|
| Improvementb | 53% | 25% | 64% | 35% |
| No Improvement | 37% | 67% | 29% | 63% |
| Missing/Unassessable Data | 10% | 7% | 7% | 2% |
| a Intent-to-Treat population (patients with ≥ 1
dose of study drug) with assessable baseline biopsies. b Histological improvement defined as ≥ 2 point decrease in the Knodell necro-inflammatory score with no worsening of the Knodell fibrosis score. |
||||
Table 5 illustrates the changes in Ishak Fibrosis Score by treatment group.
Table 5: Changes in Ishak Fibrosis Score at Week 48
| Number of Adequate Biopsy Pairs | Study 437 | Study 438 | ||
| HEPSERA (adefovir dipivoxil) 10 mg (N=152) |
Placebo (N=149) |
HEPSERA (adefovir dipivoxil) 10 mg (N=113) |
Placebo (N=56) |
|
| Ishak Fibrosis ScoreImproveda | 34% | 19% | 34% | 14% |
| Unchanged | 55% | 60% | 62% | 50% |
| Worsened* | 11% | 21% | 4% | 36% |
| a Change of 1 point or more in Ishak Fibrosis Score. | ||||
At Week 48, improvement was seen with respect to mean change in serum HBV DNA (log10 copies/mL), normalization of ALT, and HBeAg seroconversion as compared to placebo in patients receiving HEPSERA (adefovir dipivoxil) (Table 6).
Table 6: Change in Serum HBV DNA, ALT Normalization, and
HBeAg Seroconversion at Week 48
| Study 437 | Study 438 | |||
| HEPSERA (adefovir dipivoxil) 10 mg (N=171) |
Placebo (N=167) |
HEPSERA (adefovir dipivoxil) 10 mg (N=123) |
Placebo (N=61) |
|
| Mean change ± SD in serum HBV DNA from baseline (log10 copies/mL) | -3.57 ± 1.64 | -0.98 ± 1.32 | -3.65 ± 1.14 | -1.32 ± 1.25 |
| ALT normalization | 48% | 16% | 72% | 29% |
| HBeAg seroconversion | 12% | 6% | NAa | NAa |
| a Patients with HBeAg-negative disease cannot undergo HBeAg seroconversion. | ||||
In Study 437, continued treatment with HEPSERA (adefovir dipivoxil) to 72 weeks resulted in continued maintenance of mean reductions in serum HBV DNA observed at Week 48. An increase in the proportion of patients with ALT normalization was also observed in Study 437. The effect of continued treatment with HEPSERA (adefovir dipivoxil) on seroconversion is unknown.
In Study 438, patients who received HEPSERA (adefovir dipivoxil) during the first 48 weeks were re-randomized in a blinded manner to continue on HEPSERA (adefovir dipivoxil) or receive placebo for an additional 48 weeks. At Week 96, 50 of 70 (71%) of patients who continued treatment with HEPSERA (adefovir dipivoxil) had undetectable HBV DNA levels ( < 1000 copies/mL), and 47 of 64 (73%) of patients had ALT normalization. HBV DNA and ALT levels returned towards baseline in most patients who stopped treatment with HEPSERA (adefovir dipivoxil) .
From 141 eligible patients, there were 125 (89%) patients in Study 438 who chose to continue HEPSERA (adefovir dipivoxil) for up to 192 weeks or 240 weeks (4 years or 5 years). As these patients had already received HEPSERA (adefovir dipivoxil) for at least 48 weeks and appeared to be experiencing a benefit, they are not necessarily representative of patients initiating HEPSERA (adefovir dipivoxil) . Of these patients, 89/125 (71%) and 47/70 (67%) had an undetectable HBV DNA level ( < 1000 copies/mL) at Week 192 and Week 240, respectively. Of the patients who had an elevated ALT at baseline, 77/104 (74%) and 42/64 (66%) had a normal ALT at Week 192 and Week 240, respectively. Six (5%) patients experienced HBsAg loss.
HEPSERA (adefovir dipivoxil) was also evaluated in an open-label, uncontrolled study of 467 chronic hepatitis B patients pre- (N=226) and post- (N=241) liver transplantation with clinical evidence of lamivudine- resistant hepatitis B virus (Study 435). At baseline, 60% of pre-liver transplantation patients were classified as Child-Pugh-Turcotte score of Class B or C. The median baseline HBV DNA as measured by the Roche Amplicor Monitor PCR assay (LLOQ = 1000 copies/mL) was 7.4 and 8.2 log10 copies/mL, and the median baseline ALT was 1.8 and 2.0 times the upper limit of normal in pre- and post-liver transplantation patients, respectively. Results of this study are displayed in Table 5. Treatment with HEPSERA (adefovir dipivoxil) resulted in a similar reduction in serum HBV DNA regardless of the patterns of lamivudine-resistant HBV DNA polymerase mutations at baseline. The significance of the efficacy results listed in Table 7 as they relate to clinical outcomes is not known.
Table 7: Efficacy in Pre- and Post-Liver Transplantation
Patients at Week 48
| Efficacy Parametera | Pre-Liver Transplantation (N=226) |
Post-Liver Transplantation (N=241) |
| Mean change ± SD in HBV DNA from baseline (log10 copies/mL) | -3.7 ± 1.6 (n=117) | -4.0 ± 1.6 (n=164) |
| Proportion with undetectable HBV DNA ( < 1000 copies/mL)b | 77/109 (71%) | 64/159 (40%) |
| Stable or improved Child-Pugh-Turcotte score | 86/90 (96%) | 107/115 (93%) |
| Normalization of:c ALT | 61/82 (74%) | 56/110 (51%) |
| Albumin | 43/54 (80%) | 21/26 (81%) |
| Bilirubin | 38/68 (58%) | 29/38 (76%) |
| Prothrombin time | 39/46 (85%) | 5/9 (56%) |
| a Data are missing for 29% (HBV DNA) and 37% to
45% (CPT Score, Normalization of ALT, Albumin, Bilirubin, and PT) of total
patients enrolled in the study. b Denominator is the number of patients with serum HBV DNA ≥ 1000 copies/mL at baseline using the Roche Amplicor Monitor PCR Assay (LLOQ = 1000 copies/mL) and non-missing value at Week 48. c Denominator is patients with abnormal values at baseline and non-missing value at Week 48. |
||
In Study 461, a double-blind, active controlled study in 59 chronic hepatitis B patients with clinical evidence of lamivudine-resistant hepatitis B virus, patients were randomized to receive either HEPSERA (adefovir dipivoxil) monotherapy or HEPSERA (adefovir dipivoxil) in combination with lamivudine 100 mg or lamivudine 100 mg alone. At Week 48, the mean ± SD decrease in serum HBV DNA as measured by the Roche Amplicor Monitor PCR assay (LLOQ = 1000 copies/mL) was 4.00 ± 1.41 log10 copies/mL for patients treated with HEPSERA (adefovir dipivoxil) and 3.46 ± 1.10 log10 copies/mL for patients treated with HEPSERA (adefovir dipivoxil) in combination with lamivudine. There was a mean decrease in serum HBV DNA of 0.31 ± 0.93 log10 copies/mL in patients receiving lamivudine alone. ALT normalized in 47% of patients treated with HEPSERA (adefovir dipivoxil) , in 53% of patients treated with HEPSERA (adefovir dipivoxil) in combination with lamivudine, and 5% of patients treated with lamivudine alone. The significance of these findings as they relate to clinical outcomes is not known.
Study 518 was a double-blind, placebo-controlled, study in which 173 pediatric patients (ages 2 to < 18 years) with chronic hepatitis B (CHB) infection and elevated ALT were randomized 2:1 (115 receiving adefovir dipivoxil and 58 receiving placebo). Randomization was stratified by prior treatment and age 2 to < 7 years old (cohort 1), 7 to < 12 years old (cohort 2), and 12 to < 18 years old (cohort 3). All patients in cohort 3 received 10 mg tablet formulation; all patients in cohorts 1 and 2 received an investigational suspension formulation (0.3 mg/kg/day cohort 1, 0.25 mg/kg/day cohort 2) once daily. The primary efficacy endpoint was HBV DNA < 1000 copies/mL plus normalization of ALT at the end of Week 48.
In cohort 3 (n=83), significantly more patients treated with HEPSERA (adefovir dipivoxil) achieved the primary efficacy endpoint at the end of 48 weeks of blinded treatment (23%) when compared to placebo-treated patients (0%). The proportion of patients from cohorts 1 and 2 who responded to treatment with adefovir dipivoxil was not statistically significant when compared to the placebo arm, although the adefovir plasma concentrations in these patients were comparable to those observed in older patients. Overall, 22 of 115 (19%) of pediatric patients who received adefovir dipivoxil vs. 1 of 58 (2%) of placebo treated patients responded to treatment by Week 48 [see ADVERSE REACTIONS, Use In Special Populations].
Last reviewed on RxList: 11/5/2009
This monograph has been modified to include the generic and brand name in many instances.
Here is a collection of user reviews for the medication Hepsera sorted by most helpful.
Report Problems to the Food and Drug Administration
You are encouraged to report negative side effects of prescription drugs to the FDA. Visit the FDA MedWatch website or call 1-800-FDA-1088.
Find the secrets to longer life.
Copyright © 2012 by WebMD, LLC.
RxList does not provide medical advice, diagnosis or treatment. See additional information.
Updated & New