Alefacept (3586)
[ a-la-fa'-cept ]
| Ingredients: |
Alefacept |
| Indications: |
Psoriasis |
| Pregnancy Category: |
B |
| FDA Approved: |
2003- 01- 01 |
| Classes: |
Immunosuppressives |
| HCFA Jcodes: |
J0215 |
| Brand Names: |
Amevive
-
US; Israel
;
|
| DEA schedules: |
(none)
|
| Cost of therapy: |
$11,940.00
(
Plaque Psoriasis ;
Amevive ;
15 mg/vial ;
15 mg/week ;
84 day supply
)
|
DESCRIPTION
|
| |
Amevive (alefacept) is an immunosuppressive dimeric fusion protein that consists of the extracellular CD2- binding portion
of the human leukocyte function antigen- 3 (LFA- 3) linked to the Fc (hinge, CH 2 and CH 3 domains) portion of human IgG1. Alefacept isproduced by recombinant DNA technology in a Chinese Hamster Ovary (CHO) mammalian
cell expression system. The molecular weight of alefacept is 91.4 kilodaltons.
Amevive is supplied as a sterile, white- to- off- white, preservative- free, lyophilized powder for parenteral administration.
After reconstitution with 0.6 ml of the supplied sterile water for injection, the solution of Amevive is clear, with a pH
of approximately 6.9.
Amevive is available in 2 formulations. Amevive for intramuscular (IM) injection contains 15 mg alefacept per 0.5 ml of reconstituted
solution. Amevive for intravenous (IV) injection contains 7.5 mg alefacept per 0.5 ml of reconstituted solution. Both formulations
also contain 12.5 mg sucrose, 5.0 mgglycine, 3.6 mg sodium citrate dihydrate, and 0.06 mg citric acid monohydrate per 0.5
ml.
|
CLINICAL PHARMACOLOGY
|
| |
Alefacept interferes with lymphocyte activation by specifically binding to the lymphocyte antigen, CD2, and inhibiting LFA-
3/ CD2 interaction. Activation of T lymphocytes involving the interaction between LFA- 3 on antigen- presenting cells and
CD2 on T lymphocytes plays a role in the pathophysiology ofchronic plaque psoriasis. The majority of T lymphocytes in psoriatic
lesions are of the memory effector phenotype characterized by the presence of the CD45RO marker, 1 express activation markers ( e.g., CD25, CD69) and release inflammatory cytokines, such as interferon γ.
Alefacept also causes a reduction in subsets of CD2+ T lymphocytes (primarily CD45RO+), presumably by bridging between CD2
on target lymphocytes and immunoglobulin Fc receptors on cytotoxic cells, such as natural killer cells. Treatment with alefacept
results in a reduction in circulating total CD4+and CD8+ T lymphocyte counts. CD2 is also expressed at low levels on the surface
of natural killer cells and certain bone marrow B lymphocytes. Therefore, the potential exists for alefacept to affect the
activation and numbers of cells other than T lymphocytes. In clinical studies of alefacept, minor changesin the numbers of
circulating cells other than T lymphocytes have been observed.
Pharmacokinetics
|
| |
In patients with moderate to severe plaque psoriasis, following a 7.5 mg IV administration, the mean volume of distribution
of alefacept was 94 ml/ kg, the mean clearance was 0.25 ml/ h/ kg, and the mean elimination half- life was approximately 270
hours. Following an IM injection, bioavailability was 63%.
The pharmacokinetics of alefacept in pediatric patients have not been studied. The effects of renal or hepatic impairment
on the pharmacokinetics of alefacept have not been studied.
|
Pharmacodynamics
|
| |
At doses tested in clinical trials, alefacept therapy resulted in a dose- dependent decrease in circulating total lymphocytes. 2 This reduction predominantly affected the memory effector subset of the CD4+ and CD8+ T lymphocyte compartments(CD4+CD45RO+
and CD8+CD45RO+), the predominant phenotype in psoriatic lesions. Circulating naïve T lymphocyte and natural killer cell counts
appeared to be only minimally susceptible to alefacept treatment, while circulating B lymphocyte counts appeared not to be
affected by alefacept (see ADVERSE REACTIONS, Effect on Lymphocyte Counts ).
|
|
CLINICAL STUDIES
|
| |
Alefacept was evaluated in two randomized, double- blind, placebo- controlled studies in adults with chronic (≥1 year) plaque
psoriasis and a minimum body surface area involvement of 10% who were candidates for or had previously received systemic therapy
or phototherapy. Each course consisted of once- weeklyadministration for 12 weeks (IV for Study 1, IM for Study 2) of placebo
or alefacept. Patients could receive concomitant low potency topical steroids. Concomitant phototherapy or systemic therapy
was not allowed.
In Study 1, patients were randomized to receive 1 or 2 courses of alefacept 7.5 mg administered by IV bolus. The first and
second courses in the 2 course cohort were separated by at least a 12 week post- dosing interval. A total of 553 patients
were randomized into three cohorts ( TABLE 1 ).
| TABLE 1
Treatment Group and Number of Patients Dosed in Study 1
|
| |
Course 1 |
Course 2 |
| Cohort 1 |
Alefacept (n=183) |
Alefacept (n=154) |
| Cohort 2 |
Alefacept (n=184) |
Placebo (n=142) |
| Cohort 3 |
Placebo (n=186) |
Alefacept (n=153) |
|
Study 2 provided a basis for comparison of patients treated with either 10 or 15 mg alefacept IM. One hundred seventy- three
(173) patients were randomized to receive 10 mg of alefacept IM, 166 to receive 15 mg of alefacept IM, and 168 to receive
placebo.
In Studies 1 and 2, 77% of patients had previously received systemic therapy and/ or phototherapy for psoriasis. Of these,
23% and 19%, respectively, had failed to respond to at least 1 of these previous therapies.
TABLE 2 shows the treatment response in the first course of Study 1 and Study 2. Response to treatment in both studies was defined
as the proportion of patients with a reduction in score on the Psoriasis Area and Severity Index (PASI) 3 of at least 75% from baseline at 2 weeks following the 12 week treatment period.
Other treatment responses included the proportion of patients who achieved a scoring of "almost clear" or "clear" by Physician
Global Assessment (PGA) and the proportion of patients with a reduction in PASI of at least 50% from baseline 2 weeks after
the 12 week treatment period.
| TABLE 2
Percentage of Patients Responding to the First Course of Treatment in Study 1 (The IV Study) and Study 2 (The IM Study) 2
Weeks Post- Dosing
|
| |
Treatment Response: (Reduction in Disease Activity From Baseline) |
| |
≥75% Reduction PASI |
≥50% Reduction PASI |
PGA "Almost Clear" or "Clear" |
| Study 1
|
| Placebo (n=186) |
4% |
10% |
4% |
| Alefacept 7.5 mg IV (n=367)* |
14% |
38% |
11% |
| Difference (95% CI) |
10† (6, 15) |
28† (22, 35) |
7‡ (3, 12) |
| Study 2
|
| Placebo (n=168) |
5% |
18% |
5% |
| Alefacept 15 mg IM (n=166) |
21% |
42% |
14% |
| Difference (95% CI) |
16† (9, 23) |
24† (14, 33) |
9§ (3, 15) |
|
| *
|
Cohorts 1 and 2 are combined. |
| †
|
p values <0.001 |
| ‡
|
p value 0.004 |
| §
|
p value 0.006 |
|
In Study 2, the proportion of responders to the 10 mg IM dose was higher than placebo, but the difference was not statistically
significant.
In both studies, onset of response to alefacept treatment (at least a 50% reduction of baseline PASI) began 60 days after
the start of therapy.
With 1 course of therapy in Study 1 (IV route), the median duration of response (defined as maintenance of a 75% or greater
reduction in PASI) was 3.5 months for alefacept- treated patients and 1 month for placebo- treated patients. In Study 2 (IM
route), the median duration of response was approximately2 months for both alefacept- treated patients and placebo- treated
patients.
Most patients who had responded to either alefacept or placebo maintained a 50% or greater reduction in PASI through the 3
month observation period.
The responders (n=52) in a subset of patients in Study 1 who crossed over to placebo for course 2 (Cohort 2) maintained a
50% or greater reduction in PASI for a median of 7 months.
Some patients achieved their maximal response beyond 2 weeks post- dosing. In Studies 1 and 2, an additional 11% (42/ 367)
and 7% (12/ 166) of patients treated with alefacept, respectively, achieved a 75% reduction from baseline PASI score at 1
or more visits after the first 2 weeks of the follow- up period.
Retreatment
|
| |
Patients in Study 1 who had completed the first IV treatment course were eligible to receive a second treatment course if
their psoriasis was less than "clear" by PGA and their CD4+ T lymphocyte count was above the lower limit of normal. The median
reduction in PASI score was greater in patients whoreceived a second course of alefacept treatment compared to patients who
received placebo.
Data on the safety and efficacy of alefacept treatment beyond 2 courses are limited.
|
|
INDICATIONS AND USAGE
|
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Alefacept is indicated for the treatment of adult patients with moderate to severe chronic plaque psoriasis who are candidates
for systemic therapy or phototherapy.
|
CONTRAINDICATIONS
|
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Alefacept should not be administered to patients with known hypersensitivity to alefacept or any of its components.
|
WARNINGS
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Lymphopenia
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AMEVIVE INDUCES DOSE- DEPENDENT REDUCTIONS IN CIRCULATING CD4+ AND CD8+ T LYMPHOCYTE COUNTS.
A COURSE OF AMEVIVE THERAPY SHOULD NOT BE INITIATED IN PATIENTS WITH A CD4+ T LYMPHOCYTE COUNT BELOW NORMAL. THE CD4+ T LYMPHOCYTE
COUNTS OF PATIENTS RECEIVING AMEVIVE SHOULD BE MONITORED WEEKLY THROUGHOUT THE COURSE OF THE 12 WEEK DOSING REGIMEN. DOSING
SHOULD BE WITHHELD IF CD4+ T LYMPHOCYTECOUNTS ARE BELOW 250 CELLS/ μl. THE DRUG SHOULD BE DISCONTINUED IF THE COUNTS REMAIN
BELOW 250 CELLS/ μl FOR 1 MONTH (SEE DOSAGE AND ADMINISTRATION ).
|
Malignancies
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| |
Alefacept may increase the risk of malignancies. Some patients who received alefacept in clinical studies developed malignancies
(see ADVERSE REACTIONS, Malignancies ). In preclinical studies, animals developed B cell hyperplasia, and 1 animal developed a lymphoma (see PRECAUTIONS, Carcinogenesis, Mutagenesis, and Impairment of Fertility ).Alefacept should not be administered to patients with a history of systemic malignancy. Caution should be exercised when
considering the use of alefacept in patients at high risk for malignancy. If a patient develops a malignancy, alefacept should
be discontinued.
|
Serious Infections
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Alefacept is an immunosuppressive agent and, therefore, has the potential to increase the risk of infection and reactivate
latent, chronic infections. Alefacept should not be administered to patients with a clinically important infection. Caution
should be exercised when considering the use of alefaceptin patients with chronic infections or a history of recurrent infection.
Patients should be monitored for signs and symptoms of infection during or after a course of alefacept. New infections should
be closely monitored. If a patient develops a serious infection, alefacept should be discontinued (see ADVERSE REACTIONS, Infections ).
|
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PRECAUTIONS
|
| |
Effects on the Immune System
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Patients receiving other immunosuppressive agents or phototherapy should not receive concurrent therapy with alefacept because
of the possibility of excessive immunosuppression. The duration of the period following treatment with alefacept before one
should consider starting other immunosuppressivetherapy has not been evaluated.
The safety and efficacy of vaccines, specifically live or live- attenuated vaccines, administered to patients being treated
with alefacept have not been studied. In a study of 46 patients with chronic plaque psoriasis, the ability to mount immunity
to tetanus toxoid (recall antigen) and an experimentalneo- antigen was preserved in those patients undergoing alefacept therapy.
|
Allergic Reactions
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Hypersensitivity reactions (urticaria, angioedema) were associated with the administration of alefacept. If an anaphylactic
reaction or other serious allergic reaction occurs, administration of alefacept should be discontinued immediately and appropriate
therapy initiated.
|
Information for the Patient
|
| |
Patients should be informed of the need for regular monitoring of white blood cell (lymphocyte) counts during therapy and
that alefacept must be administered under the supervision of a physician. Patients should also be informed that alefacept
reduces lymphocyte counts, which could increase their chancesof developing an infection or a malignancy. Patients should be
advised to inform their physician promptly if they develop any signs of an infection or malignancy while undergoing a course
of treatment with alefacept.
Female patients should also be advised to notify their physicians if they become pregnant while taking alefacept (or within
8 weeks of discontinuing alefacept) and be advised of the existence of and encouraged to enroll in the Pregnancy Registry.
Call 1- 866- Amevive (1- 866- 263- 8483) to enroll into theRegistry (see Pregnancy Category B ).
|
Laboratory Tests
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CD4+ T lymphocyte counts should be monitored weekly during the 12 week dosing period and used to guide dosing. Patients should
have normal CD4+ T lymphocyte counts prior to an initial or a subsequent course of treatment with alefacept. Dosing should
be withheld if CD4+ T lymphocyte counts are below250 cells/ μl. Alefacept should be discontinued if CD4+ T lymphocyte counts
remain below 250 cells/ μl for 1 month.
|
Carcinogenesis, Mutagenesis, and Impairment of Fertility
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| |
In a chronic toxicity study, cynomolgus monkeys were dosed weekly for 52 weeks with IV alefacept at 1 mg/ kg/ dose or 20 mg/
kg/ dose. One animal in the high dose group developed a B- cell lymphoma that was detected after 28 weeks of dosing. Additional
animals in both dose groups developed B- cell hyperplasiaof the spleen and lymph nodes.
All animals in the study were positive for an endemic primate gammaherpes virus also known as lymphocryptovirus (LCV). Latent
LCV infection is generally asymptomatic, but can lead to B- cell lymphomas when animals are immune suppressed.
In a separate study, baboons given 3 doses of alefacept at 1 mg/ kg every 8 weeks were found to have centroblast proliferation
in B- cell dependent areas in the germinal centers of the spleen following a 116 day washout period.
The role of alefacept in the development of the lymphoid malignancy and the hyperplasia observed in non- human primates and
the relevance to humans is unknown. Immunodeficiency- associated lymphocyte disorders (plasmacytic hyperplasia, polymorphic
proliferation, and B- cell lymphomas) occur in patientswho have congenital or acquired immunodeficiencies including those
resulting from immunosuppressive therapy.
No carcinogenicity or fertility studies were conducted.
Mutagenicity studies were conducted in vitro and in vivo; no evidence of mutagenicity was observed.
|
Pregnancy Category B
|
| |
Women of childbearing potential make up a considerable segment of the patient population affected by psoriasis. Since the
effect of alefacept on pregnancy and fetal development, including immune system development, is not known, health care providers
are encouraged to enroll patients currently takingalefacept who become pregnant into the Biogen Pregnancy Registry by calling
1- 866- Amevive (1- 866- 263- 8483).
Reproductive toxicology studies have been performed in cynomolgus monkeys at doses up to 5 mg/ kg/ week (about 62 times the
human dose based on body weight) and have revealed no evidence of impaired fertility or harm to the fetus due to alefacept.
No abortifacient or teratogenic effects were observedin cynomolgus monkeys following IV bolus injections of alefacept administered
weekly during the period of organogenesis to gestation. Alefacept underwent trans- placental passage and produced in utero exposure in the developing monkeys. In utero, serum levels of exposure in these monkeys were 23% of maternal serum levels. No evidence of fetal toxicity including adverse
effects on immune system development was observed in any of these animals.
Animal reproduction studies, however, are not always predictive of human response and there are no adequate and well- controlled
studies in pregnant women. Because the risk to the development of the fetal immune system and postnatal immune function in
humans is unknown, alefacept should be used duringpregnancy only if clearly needed. If pregnancy occurs while taking alefacept,
continued use of the drug should be assessed.
|
Nursing Mothers
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It is not known whether alefacept is excreted in human milk. Because many drugs are excreted in human milk, and because there
exists the potential for serious adverse reactions in nursing infants from alefacept, a decision should be made whether to
discontinue nursing while taking the drug or to discontinuethe use of the drug, taking into account the importance of the
drug to the mother.
|
Geriatric Use
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| |
Of the 1357 patients who received alefacept in clinical trials, a total of 100 patients were ≥65 years of age and 13 patients
were ≥75 years of age. No differences in safety or efficacy were observed between older and younger patients, but there were
not sufficient data to exclude important differences. Because the incidence of infections and certain malignancies is higher
in the elderly population, in general, caution should be used in treating the elderly.
|
Pediatric Use
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| |
The safety and efficacy of alefacept in pediatric patients have not been studied. Alefacept is not indicated for pediatric
patients.
|
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DRUG INTERACTIONS
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No formal interaction studies have been performed. The duration of the period following treatment with alefacept before one
should consider starting other immunosuppressive therapy has not been evaluated.
|
ADVERSE REACTIONS
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The most serious adverse reactions were:
Commonly observed adverse events seen in the first course of placebo- controlled clinical trials with at least a 2% higher
incidence in the alefacept- treated patients compared to placebo- treated patients were: pharyngitis, dizziness, increased
cough, nausea, pruritus, myalgia, chills, injection sitepain, injection site inflammation, and accidental injury. The only
adverse event that occurred at a 5% or higher incidence among alefacept- treated patients compared to placebo- treated patients
was chills (1% placebo versus 6% alefacept), which occurred predominantly with IV administration.
The adverse reactions which most commonly resulted in clinical intervention were cardiovascular events including coronary
artery disorder in <1% of patients and myocardial infarct in <1% of patients. These events were not observed in any of the
413 placebo- treated patients. The total number ofpatients hospitalized for cardiovascular events in the alefacept- treated
group was 1.2% (11/ 876).
The most common events resulting in discontinuation of treatment with alefacept were CD4+ T lymphocyte levels below 250 cells/
μl (see WARNINGS and ADVERSE REACTIONS, Effect on Lymphocyte Counts ), headache (0.2%), and nausea (0.2%).
Because clinical trials are conducted under widely varying conditions, adverse event rates observed in the clinical trials
of a drug cannot be directly compared to rates in the clinical trials of another drug and may not reflect the rates observed
in practice. The adverse reaction information does, however, provide a basis for identifying the adverse events that appear
to be related to drug use and a basis for approximating rates.
The data described below reflect exposure to alefacept in a total of 1357 psoriasis patients, 85% of whom received 1- 2 courses
of therapy and the rest received 3- 6 courses and were followed for up to 3 years. Of the 1357 total patients, 876 received
their first course in placebo- controlled studies. The population studied ranged in age from 16- 84 years, and included 69%
men and 31% women. The patients were mostly Caucasian (89%), reflecting the general psoriatic population. Disease severity
at baseline was moderate to severe psoriasis.
Effect on Lymphocyte Counts
|
| |
In the IM study (Study 2), 4% of patients temporarily discontinued treatment and no patients permanently discontinued treatment
due to CD4+ T lymphocyte counts below the specified threshold of 250 cells/ μl. In Study 2, 10%, 28%, and 42% of patients
had total lymphocyte, CD4+, and CD8+ T lymphocytecounts below normal, respectively. Twelve weeks after a course of therapy
(12 weekly doses), 2%, 8%, and 21% of patients had total lymphocyte, CD4+, and CD8+ T cell counts below normal.
In the first course of the IV study (Study 1), 10% of patients temporarily discontinued treatment and 2% permanently discontinued
treatment due to CD4+ T lymphocyte counts below the specified threshold of 250 cells/ μl. During the first course of Study
1, 22% of patients had total lymphocyte countsbelow normal, 48% had CD4+ T lymphocyte counts below normal and 59% had CD8+
T lymphocyte counts below normal. The maximal effect on lymphocytes was observed within 6- 8 weeks of initiation of treatment.
Twelve weeks after a course of therapy (12 weekly doses), 4% of patients had total lymphocyte counts belownormal, 19% had
CD4+ T lymphocyte counts below normal, and 36% had CD8+ T lymphocyte counts below normal.
For patients receiving a second course of alefacept in Study 1, 17% of patients had total lymphocyte counts below normal,
44% had CD4+ T lymphocyte counts below normal, and 56% had CD8+ T lymphocyte counts below normal. Twelve weeks after completing
dosing, 3% of patients had total lymphocyte countsbelow normal, 17% had CD4+ T lymphocyte counts below normal, and 35% had
CD8+ T lymphocyte counts below normal (see WARNINGS , and PRECAUTIONS, Laboratory Tests ).
|
Malignancies
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| |
In the 24 week period constituting the first course of placebo- controlled studies, 13 malignancies were diagnosed in 11 alefacept-
treated patients. The incidence of malignancies was 1.3% (11/ 876) for alefacept- treated patients compared to 0.5% (2/ 413)
in the placebo group.
Among 1357 patients who received alefacept, 25 patients were diagnosed with 35 treatment- emergent malignancies. The majority
of these malignancies (23 cases) were basal (6) or squamous cell cancers (17) of the skin. Three cases of lymphoma were observed;
1 was classified as non- Hodgkin's follicle- centercell lymphoma and 2 were classified as Hodgkin's disease.
|
Infections
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| |
In the 24 week period constituting the first course of placebo- controlled studies, serious infections (infections requiring
hospitalization) were seen at a rate of 0.9% (8/ 876) in alefacept- treated patients and 0.2% (1/ 413) in the placebo group.
In patients receiving repeated courses of alefacept therapy, the rates of serious infections were 0.7% (5/ 756) and 1.5% (3/
199) in the second and third course of therapy, respectively. Serious infections among 1357 alefacept- treated patients included
necrotizing cellulitis, peritonsillar abscess, post- operative and burn wound infection, toxic shock, pneumonia, appendicitis,
pre- septal cellulitis, cholecystitis, gastroenteritis and herpes simplex infection.
|
Hypersensitivity Reactions
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| |
In clinical studies 2 patients were reported to experience angioedema, 1 of whom was hospitalized. In the 24 week period constituting
the first course of placebo- controlled studies, urticaria was reported in 6 (<1%) alefacept- treated patients versus 1 patient
in the control group. Urticaria resultedin discontinuation of therapy in 1 of the alefacept- treated patients.
|
Injection Site Reactions
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| |
In the IM study (Study 2), 16% of alefacept- treated patients and 8% of placebo- treated patients reported injection site
reactions. Reactions at the site of injection were generally mild, typically occurred on single occasions, and included either
pain (7%), inflammation (4%), bleeding (4%), edema (2%), non- specific reaction (2%), mass (1%), or skin hypersensitivity
(<1%). In the clinical trials, a single case of injection site reaction led to the discontinuation of alefacept.
|
Immunogenicity
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| |
Approximately 3% (35/ 1306) of patients receiving alefacept developed low- titer antibodies to alefacept. No apparent correlation
of antibody development and clinical response or adverse events was observed. The long- term immunogenicity of alefacept is
unknown.
The data reflect the percentage of patients whose test results were considered positive for antibodies to alefacept in an
ELISA assay, and are highly dependent on the sensitivity and specificity of the assay. Additionally, the observed incidence
of antibody positivity in an assay may be influenced byseveral factors including sample handling, timing of sample collection,
concomitant medications, and underlying disease. For these reasons, comparison of the incidence of antibodies to alefacept
with the incidence of antibodies to other products may be misleading.
|
Other Observed Adverse Reactions From Clinical Trials
|
| |
Less common events that were observed at a higher rate in alefacept- treated patients include rare cases (9) of transaminase
elevations to 5- 10 times the upper limit of normal.
|
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OVERDOSAGE
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The highest dose tested in humans (0.75 mg/ kg IV) was associated with chills, headache, arthralgia, and sinusitis within
1 day of dosing. Patients who have been inadvertently administered an excess of the recommended dose should be closely monitored
for effects on total lymphocyte count and CD4+ T lymphocytecount.
|
DOSAGE AND ADMINISTRATION
|
| |
Alefacept should only be used under the guidance and supervision of a physician.
The recommended dose of alefacept is 7.5 mg given once weekly as an IV bolus or 15 mg given once weekly as an IM injection.
The recommended regimen is a course of 12 weekly injections. Retreatment with an additional 12 week course may be initiated
provided that CD4+ T lymphocyte counts are within thenormal range, and a minimum of a 12 week interval has passed since the
previous course of treatment. Data on retreatment beyond 2 cycles are limited.
The CD4+ T lymphocyte counts of patients receiving alefacept should be monitored weekly before initiating dosing and throughout
the course of the 12 week dosing regimen. Dosing should be withheld if CD4+ T lymphocyte counts are below 250 cells/ μl. The
drug should be discontinued if the counts remainbelow 250 cells/ μl for 1 month (see PRECAUTIONS, Laboratory Tests ).
Preparation Instructions
|
| |
Alefacept should be reconstituted by a health care professional using aseptic technique. Each vial is intended for single
patient use only.
Do not add other medications to solutions containing alefacept. Do not reconstitute alefacept with other diluents. Do not
filter reconstituted solution during preparation or administration.
Following reconstitution, the product should be used immediately or within 4 hours if stored in the vial at 2- 8°C (36- 46°F).
ALEFACEPT NOT USED WITHIN 4 HOURS OF RECONSTITUTION SHOULD BE DISCARDED.
|
Administration Instructions
|
| |
For IM use, inject the full 0.5 ml of solution. Rotate injection sites so that a different site is used for each new injection. New injections
should be given at least 1 inch from an old site and never into areas where the skin is tender, bruised, red, or hard.
|
|
References
|
| |
1. Bos JD, Hagenaars C, Das PK, et al. Predominance of "memory" T cells (CD4+, CDw29+) over "naïve" T cells (CD4+, CD45R+) in both normal and diseased human skin.
Arch Dermatol Res 1989; 281:24- 30.
2. Ellis C, Krueger GG. Treatment of chronic plaque psoriasis by selective targeting of memory effector T lymphocytes. N Engl
J Med 2001; 345:248- 255.
3. Fredriksson T, Pettersson U. Severe psoriasis — oral therapy with a new retinoid. Dermatologica 1978; 157:238- 244.
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HOW SUPPLIED
|
| |
Amevive for IV administration is supplied in either a carton containing 4 administration dose packs, or in a carton containing
1 administration dose pack. Each dose pack contains one 7.5 mg single- use vial of Amevive, one 10 ml single- use diluent
vial (sterile water for injection), 1 syringe, one 23gauge, ¾ inch winged infusion set, and two 23 gauge, 1¼ inch needles.
Amevive for IM administration is supplied in either a carton containing 4 administration dose packs, or in a carton containing
1 administration dose pack. Each dose pack contains one 15 mg single- use vial of Amevive, one 10 ml single- use diluent vial
(sterile water for injection), 1 syringe, and two23 gauge, 1¼ inch needles.
Amevive is reconstituted with 0.6 ml of the 10 ml single- use diluent.
Storage: The dose tray containing Amevive (lyophilized powder) should be stored at controlled room temperature (15- 30°C; 59- 86°F).
PROTECT FROM LIGHT. Retain in carton until time of use.
|
PRODUCT IDENTIFICATION
|
| |
None Available |
PRODUCT LISTING - EQUIVALENTS NOT AVAILABLE
|
| |
| powder for injection - intramuscular - 15 mg -
|
| 1.0 |
$995.00 |
Amevive
Biogen Inc
|
59627002104 |
| 4.0 |
$3980.00 |
Amevive
Biogen Inc
|
59627002103 |
| powder for injection - intravenous - 7.5 mg -
|
| 1.0 |
$1029.60 |
Amevive
Biogen Inc
|
59627002002 |
| 4.0 |
$2800.00 |
Amevive
Biogen Inc
|
59627002001 |
|
|