Adbry Autoinjector (tralokinumab-ldrm)
Eczema Agents Systemic Interleukin-13 (IL-13)Antag.mAb Subcutaneous Auto-Injector (Ml)
Last reviewed · Source: First Databank (FDB) drug data
Overview
Tralokinumab-ldrm is a human IgG4 monoclonal antibody that specifically binds to human interleukin-13 (IL-13).
Tralokinumab-ldrm is a human IgG4 monoclonal antibody that specifically binds to human interleukin-13 (IL-13) and inhibits its interaction with the IL-13 receptor alpha1 and alpha2 subunits (IL-13Ralpha1 and IL-13Ralpha2). IL-13 is a naturally occurring cytokine of the type 2 immune response. Tralokinumab inhibits the bioactivity of IL-13 by blocking IL-13 interaction with IL-13Ralpha1/IL-4Ralpha receptor complex.
Tralokinumab inhibits IL-13-induced responses including the release of proinflammatory cytokines, chemokines and IgE.
Type 2 T-helper cells and the cytokines IL-4, IL-5, and IL-13 are identified as the immune components involved in the pathogenesis of atopic dermatitis. Of these cytokines, IL-13 is the most common cytokine found in skin lesions due to atopic dermatitis. Higher IL-13 levels are correlated with greater disease severity.
The absolute bioavailability of tralokinumab following subcutaneous injection is estimated to be 76%. Peak plasma concentrations were achieved 5-8 days following subcutaneous administration. The terminal half-life of the drug is 3 weeks.
The drug is expected to be metabolized into small peptides by catabolic pathways. Tralokinumab exposure decreases with increasing body weight. The median tralokinumab exposure in patients >100 kg is expected to be 1.46-fold lower than exposure in patients <100 kg.
No clinically significant differences in the pharmacokinetics of tralokinumab were observed based on age (range: 18-92 years), sex, mild to moderate renal impairment, or mild hepatic impairment. In pediatric patients (12 to 17 years of age), the mean steady-state trough concentrations of tralokinumab were 59.6 mcg/mL and 112.8 mcg/mL following administration of 150 mg and 300 mg every other week, respectively.
USES: This medication is used to treat a skin condition called eczema (atopic dermatitis). Tralokinumab belongs to a class of drugs known as monoclonal antibodies. It works by blocking a certain natural protein in your body (interleukin-13) that may cause inflammation and swelling in eczema.
Generic name: tralokinumab-ldrm
Pronunciation: (TRAL-o-KIN-ue-mab)
Drug class: Eczema Agents Systemic Interleukin-13 (IL-13)Antag.mAb
Therapeutic class: Dermatological
Reference product & biosimilars
No reference, biosimilar or interchangeable associated with this drug.
Today’s intelligence on Adbry Autoinjector
Indications
The following indications are listed for Adbry Autoinjector:
- Atopic Dermatitis
Also known as: Atopic Eczema, Disseminated Neurodermatitis.
Dosing
No dosing information is available for this tab.
No dosing information is available for this tab.
| Drug label | Dosing type | Instructions |
|---|---|---|
| Adbry 300 Mg/2 Ml Autoinjector | Maintenance | Inject 300 mg by subcutaneous route every 2 weeks rotating injection sites. |
No dosing information is available for this tab.
Drug interactions
In a clinical trial, tralokinumab had no substantial effect on concentrations of drugs metabolized by cytochrome P450 (CYP) 1A2, 2D6, 3A4, 2C19, or 2C9.
Contraindicated Drug Combination: This drug combination is contraindicated and generally should not be dispensed or administered to the same patient.
Selected Immunosuppressive Agents/Live Vaccines; Live Bcg
SEVERITY LEVEL: 1-Contraindicated Drug Combination: This drug combination is contraindicated and generally should not be dispensed or administered to the same patient.
MECHANISM OF ACTION: A variety of disease modifying agents suppress the immune system. Immunocompromised patients may be at increased risk for uninhibited replication after administration of live, attenuated vaccines or intravesicular BCG. Immune response to vaccines may be decreased during periods of immunocompromise.(1)
CLINICAL EFFECTS: The expected serum antibody response may not be obtained and/or the vaccine may result in illness.(1) After instillation of intravesicular BCG, immunosuppression may interfere with local immune response, or increase the severity of mycobacterial infection following inadvertent systemic exposure.(2)
PREDISPOSING FACTORS: Immunosuppressive diseases (e.g. hematologic malignancies, HIV disease), treatments (e.g. radiation) and drugs may all increase the magnitude of immunodeficiency.
PATIENT MANAGEMENT: The Centers for Disease Control(CDC) Advisory Committee on Immunization Practices (ACIP) states that live-virus and live, attenuated vaccines should not be administered to patients who are immunocompromised. The magnitude of immunocompromise and associated risks should be determined by a physician.(1) For patients scheduled to receive chemotherapy, vaccination should ideally precede the initiation of chemotherapy by 14 days. Patients vaccinated while on immunosuppressive therapy or in the 2 weeks prior to starting therapy should be considered unimmunized and should be revaccinated at least 3 months after discontinuation of therapy.(1) Patients who receive anti-B cell therapies should not receive live vaccines for at least 6 months after such therapies due to a prolonged duration of immunosuppression. An exception is the Zoster vaccine, which can be given at least 1 month after receipt of anti-B cell therapies.(1) The US manufacturer of abatacept states live vaccines should not be given during or for up to 3 months after discontinuation of abatacept.(2) The US manufacturer of live BCG for intravesicular treatment of bladder cancer states use is contraindicated in immunosuppressed patients.(3) The US manufacturer of daclizumab states live vaccines are not recommended during and for up to 4 months after discontinuation of treatment.(4) The US manufacturer of guselkumab states that live vaccines should be avoided during treatment with guselkumab.(5) The US manufacturer of inebilizumab-cdon states that live vaccines are not recommended during treatment and after discontinuation until B-cell repletion. Administer all live vaccinations at least 4 weeks prior to initiation of inebilizumab-cdon.(6) The US manufacturer of ocrelizumab states that live vaccines are not recommended during treatment and until B-cell repletion occurs after discontinuation of therapy. Administer all live vaccines at least 4 weeks prior to initiation of ocrelizumab.(7) The US manufacturer of ozanimod states that live vaccines should be avoided during and for up to 3 months after discontinuation of ozanimod.(8) The US manufacturer of siponimod states that live vaccines are not recommended during treatment and for up to 4 weeks after discontinuation of treatment.(9) The US manufacturer of ustekinumab states BCG vaccines should not be given in the year prior to, during, or the year after ustekinumab therapy.(10) The US manufacturer of satralizumab-mwge states that live vaccines are not recommended during treatment and should be administered at least four weeks prior to initiation of satralizumab-mwge.(11) The US manufacturer of ublituximab-xiiy states that live vaccines are not recommended during treatment and until B-cell recovery. Live vaccines should be administered at least 4 weeks prior to initiation of ublituximab-xiiy.(12) The US manufacturer of etrasimod states that live vaccines should be avoided during and for 5 weeks after treatment. Live vaccines should be administered at least 4 weeks prior to initiation of etrasimod.(13) The US manufacturer of emapalumab-lzsg states that live vaccines should not be administered to patients receiving emapalumab-lzsg and for at least 4 weeks after the last dose of emapalumab-lzsg. The safety of immunization with live vaccines during or following emapalumab-lzsg therapy has not been studied.(14) The US manufacturer of sibeprenlimab-szsi states live vaccines should not be given within 30 days prior to initiation or during treatment with sibeprenlimab-szsi.(15)
DISCUSSION: Killed or inactivated vaccines do not pose a danger to immunocompromised patients.(1) Patients with a history of leukemia who are in remission and have not received chemotherapy for at least 3 months are not considered to be immunocompromised.(1)
Severe Interaction: Action is required to reduce the risk of severe adverse interaction.
Igg Antibodies And Derivatives/Efgartigimod-Alfa
SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction.
MECHANISM OF ACTION: The neonatal Fc receptor (FcRn) prevents catabolism and mediates recycling of IgG and albumin, which leads to their long persistence in the body.(1,2) Efgartigimod-alfa binds to FcRn and may decrease systemic exposure of other ligands of FcRn, like immunoglobulins and IgG-based antibodies.(3)
CLINICAL EFFECTS: The effectiveness of medicines that bind to FcRn may be decreased.(3)
PREDISPOSING FACTORS: None determined.
PATIENT MANAGEMENT: The manufacturer of efgartigimod-alfa states that efgartigimod-alfa should not be combined with long-term use of FcRn-binding medications. If the medication is essential for the patient, efgartigimod-alfa should be discontinued.(3)
DISCUSSION: Clinical drug interaction studies with efgartigimod-alfa have not been performed. Efgartigimod-alfa may decrease concentrations of compounds that bind to the human FcRn.(3)
Igg Antibodies And Derivatives/Nipocalimab-Aahu
SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction.
MECHANISM OF ACTION: The neonatal Fc receptor (FcRn) prevents catabolism and mediates recycling of IgG and albumin, which leads to their long persistence in the body.(1,2) Nipocalimab-aahu binds to FcRn and may decrease systemic exposure of other ligands of FcRn, like immunoglobulins and IgG-based antibodies.(3)
CLINICAL EFFECTS: The effectiveness of medicines that bind to FcRn may be decreased.(3)
PREDISPOSING FACTORS: None determined.
PATIENT MANAGEMENT: The manufacturer of nipocalimab-aahu states that nipocalimab-aahu should not be combined with long-term use of FcRn-binding medications. If the medication is essential for the patient, nipocalimab-aahu should be discontinued.(3)
DISCUSSION: Clinical drug interaction studies with nipocalimab-aahu have not been performed. Nipocalimab-aahu may decrease concentrations of compounds that bind to the human FcRn.(3)
Moderate Interaction: Assess the risk to the patient and take action as needed.
Igg Antibodies And Derivatives/Rozanolixizumab-Noli
SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.
MECHANISM OF ACTION: The neonatal Fc receptor (FcRn) prevents catabolism and mediates recycling of IgG and albumin, which leads to their long persistence in the body.(1,2) Rozanolixizumab-noli binds to FcRn and may decrease systemic exposure of other ligands of FcRn, like immunoglobulins and IgG-based antibodies.(3)
CLINICAL EFFECTS: The effectiveness of medications that bind to FcRn may be decreased.(3)
PREDISPOSING FACTORS: None determined.
PATIENT MANAGEMENT: The manufacturer of rozanolixizumab-noli states that concurrent use with medications that bind to the human neonatal Fc receptor (FcRn) should be closely monitored for reduced effectiveness of these medications. If long-term use of such medications is essential for the patient, consider discontinuing rozanolixizumab-noli and use alternative therapies.(3)
DISCUSSION: Clinical drug interaction studies with rozanolixizumab-noli have not been performed. Rozanolixizumab-noli may decrease concentrations of compounds that bind to the human FcRn.(3)
Contraindications
*Known hypersensitivity to tralokinumab or any component of the formulation.
There are no contraindication contraindications for this drug.
- Parasitic infection
- Conjunctivitis
- Keratitis
Adverse reactions
There is no enhanced messaging for this drug.
Rare or Very Rare
- Anaphylaxis
- Hypersensitivity drug reaction
- Infection
- Keratitis
More Frequent
- Upper respiratory infection
Less Frequent
- Conjunctivitis
- Eosinophilia
- Injection site erythema
- Injection site sequelae
Precautions
No enhanced messaging available.
The safety and effectiveness of tralokinumab have been established for the treatment of moderate to severe atopic dermatitis in pediatric patients 12-17 years of age whose disease is not adequately controlled with topical therapies or when those therapies are not advisable; use of the drug in this age group is supported by results of a multicenter, double-blind, placebo-controlled study. Safety and efficacy have not been established in pediatric patients <12 years of age.
There are limited data on the use of tralokinumab in pregnant patients to inform a drug-associated risk of adverse developmental outcomes. Human IgG antibodies are known to cross the placental barrier; therefore, tralokinumab-ldrm may be transmitted from the mother to the developing fetus. Pregnant patients exposed to tralokinumab-ldrm should be enrolled in the pregnancy registry by calling 1-877-311-8972 or visiting https://mothertobaby.org/ongoing-study/adbry-tralokinumab/. In studies of pregnant animals receiving IV administration of tralokinumab at doses above the maximum recommended human dose, no maternal or developmental toxicity was observed.
There are no data on the presence of tralokinumab in human milk, the effects on the breast-fed infant, or the effects on milk production. Maternal IgG is present in breast milk. The effects of local GI exposure and limited systemic exposure to tralokinumab-ldrm on the breast-fed infant are unknown. Consider the developmental and health benefits of breast-feeding along with the mother's clinical need for tralokinumab and any potential adverse effects on the breast-fed child from tralokinumab or from the underlying maternal condition.
The manufacturer makes no specific dosage recommendations for geriatric patients.
Of the 1605 subjects exposed to tralokinumab in 5 atopic dermatitis trials in the initial treatment period of up to 16 weeks, 77 subjects were >=65 years of age. Clinical studies did not include sufficient numbers of subjects >=65 years of age to determine whether they respond differently from younger subjects.
ICD codes
| Code | Type | Description |
|---|---|---|
| Atopic dermatitis | ||
| L20 | ICD10CM | Atopic dermatitis |
| L20.0 | ICD10CM | Besnier's prurigo |
| L20.8 | ICD10CM | Other atopic dermatitis |
| L20.81 | ICD10CM | Atopic neurodermatitis |
| L20.82 | ICD10CM | Flexural eczema |
| L20.84 | ICD10CM | Intrinsic (allergic) eczema |
| L20.89 | ICD10CM | Other atopic dermatitis |
| L20.9 | ICD10CM | Atopic dermatitis, unspecified |
ICD code information from First Databank (FDB).
Formulary status
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Last reviewed · Source: First Databank (FDB) drug data
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