Trogarzo (ibalizumab-uiyk)
Antiretroviral - Anti-CD4 Domain 2 Monoclonal Antibody Intravenous Vial (ML)
Last reviewed · Source: First Databank (FDB) drug data
Overview
Ibalizumab-uiyk, a humanized immunoglobulin G (IgG) monoclonal antibody, is a human immunodeficiency virus (HIV) entry inhibitor. The drug is a CD4-directed post-attachment HIV type 1 (HIV-1) inhibitor.
Ibalizumab-uiyk, a recombinant humanized immunoglobulin G isotype 4 (IgG4) monoclonal antibody, is a human immunodeficiency virus (HIV) entry inhibitor. The drug is a CD4-directed post-attachment HIV type 1 (HIV-1) inhibitor that blocks HIV-1 from infecting CD4+ T cells by binding to domain 2 of CD4 and interfering with post-attachment steps required for entry of the virus particles into host cells. This prevents the viral transmission that occurs via cell-cell fusion.
Ibalizumab-uiyk does not interfere with the domain 1 binding site that is required for CD4 binding of major histocompatibility complex (MHC) class II molecules. Due to the specific binding of ibalizumab-uiyk to domain 2 of CD4, the drug blocks viral entry into the cell without altering immune functions mediated by CD4 and without causing immunosuppression. In addition, ibalizumab-uiyk does not interfere with gp120 attachment to CD4.
In the phase 3 clinical trial evaluating efficacy and safety of ibalizumab-uiyk in heavily treatment-experienced HIV-infected adults with multidrug-resistant HIV-1 infection (TMB-301), the median maximum percent inhibition (MPI) of ibalizumab-uiyk for HIV-1 isolates from 38 patients was 97% at baseline; in 10 patients who experienced treatment failure with the drug, the median MPI was 55% at the time of treatment failure. Decreased susceptibility to ibalizumab-uiyk (i.e., decreased MPI) has been observed in some patients receiving ibalizumab-uiyk and may be associated with genotypic changes in the HIV-1 envelope coding sequence that result in the loss of potential N-linked glycosylation sites (PNGS) in the V5 loop of gp120. The clinical importance of decreased susceptibility to ibalizumab-uiyk has not been established.
Known CD4 polymorphisms were analyzed to determine if any naturally occurring amino acid substitutions in the CD4 molecule potentially could affect the antiretroviral activity of ibalizumab-uiyk and results indicate that known CD4 polymorphisms appear unlikely to affect ibalizumab-uiyk binding to CD4.
There has been no evidence to date of cross-resistance between ibalizumab-uiyk and other antiretrovirals, including HIV entry and fusion inhibitors (e.g., CCR-5 co-receptor antagonists, gp41 fusion inhibitors), HIV integrase strand transfer inhibitors (INSTIs), HIV nucleoside reverse transcriptase inhibitors (NRTIs), HIV nonnucleoside reverse transcriptase inhibitors (NNRTIs), and HIV protease inhibitors (PIs), in phenotypic and genotypic testing. Ibalizumab-uiyk has been active in vitro against HIV-1 resistant to all other antiretrovirals currently commercially available in the US, including CCR5-tropic, CCRX4-tropic, and dual-tropic HIV-1. Phenotypic changes associated with ibalizumab-uiyk resistance do not alter susceptibility to other commercially available antiretrovirals and do not result in selection of CD4-independent viral isolates.
Ibalizumab-uiyk exhibits nonlinear pharmacokinetics. Following a single dose given by IV infusion over 30-90 minutes, AUC increases in a more than dose-proportional manner. As ibalizumab-uiyk dosage increased from 0.3 to 25 mg/kg, clearance of the drug decreased from 9.54 to 0.36 mL/hour per kg and elimination half-life increased from 2.7 to 64 hours.
When the recommended dosage of IV ibalizumab-uiyk (a single 2-g loading dose followed by a maintenance dosage of 800 mg once every 2 weeks) is administered, steady-state concentrations of the drug are achieved after the first 800-mg maintenance dose. The initial loading dose as an IV push administration over 90 seconds is predicted to achieve similar peak plasma concentrations and AUC relative to administration by IV infusion over 30 minutes.
USES: This drug is used with other HIV medications to help control HIV infection. It helps to decrease the amount of HIV in your body so your immune system can work better. This lowers your chance of getting HIV complications (such as new infections, cancer) and improves your quality of life.
Ibalizumab belongs to a class of drugs known as monoclonal antibodies. Ibalizumab is not a cure for HIV infection. To decrease your risk of spreading HIV disease to others, continue to take all HIV medications exactly as prescribed by your doctor.
Use an effective barrier method (latex or polyurethane condoms/dental dams) during sexual activity as directed by your doctor. Do not share personal items (such as needles/syringes, toothbrushes, and razors) that may have contacted blood or other body fluids. Consult your doctor or pharmacist for more details.
Generic name: ibalizumab-uiyk
Pronunciation: (EYE-ba-LIZ-ue-mab)
Drug class: Antiretroviral - Anti-CD4 Domain 2 Monoclonal Antibody
Therapeutic class: Anti-Infective Agents
Reference product & biosimilars
No reference, biosimilar or interchangeable associated with this drug.
Today’s intelligence on Trogarzo
Indications
The following indications are listed for Trogarzo:
- Hiv Infection
Also known as: Human Immunodeficiency Virus Disease, Human Immunodeficiency Virus Infection.
Dosing
No dosing information is available for this tab.
Ibalizumab-uiyk is administered as a single loading dose followed by maintenance doses every 2 weeks. Doses may be administered either as a diluted IV infusion or undiluted IV push.
Ibalizumab-uiyk should be administered (as an IV infusion or IV push) into the cephalic vein of the right or left arm. If the cephalic vein is not accessible, another appropriate vein may be used.
Store unopened single-dose vials containing ibalizumab-uiyk injection concentrate at 2-8degreesC, protect from light, and do not freeze. injection concentrate should appear as a colorless to slightly yellow and clear to slightly opalescent solution; do not use if it appears cloudy or discolored or contains particles.
| Drug label | Dosing type | Instructions |
|---|---|---|
| Trogarzo 200 Mg/1.33 Ml Vial | Maintenance | Infuse 800 mg over no less than 15 minute(s) by intravenous route every 2 weeks. |
No dosing information is available for this tab.
Drug interactions
Specific drug interaction studies have not been conducted to date with ibalizumab-uiyk. Based on the drug's mechanism of action and target-mediated drug disposition, the manufacturer states that drug interactions with ibalizumab-uiyk are not expected.
Contraindicated Drug Combination: This drug combination is contraindicated and generally should not be dispensed or administered to the same patient.
Anti-Retrovirals/Atidarsagene Autotemcel
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: Atidarsagene autotemcel is prepared from apheresed cells that are transduced with a replication defective, self-inactivating lentiviral vector. Antiretrovirals may interfere with the manufacturing of apheresed cells.
CLINICAL EFFECTS: Use of antiretrovirals before mobilization and apheresis may interfere with the production of atidarsagene autotemcel.
PREDISPOSING FACTORS: None determined.
PATIENT MANAGEMENT: Discontinue antiretrovirals for at least one month prior to mobilization (or the expected duration of time needed for elimination of the medication) until all cycles of apheresis are completed. If a patient requires antiretrovirals for HIV prophylaxis, then confirm a negative HIV test before beginning mobilization and apheresis of CD34+ cells.
DISCUSSION: Antiretroviral medications may interfere with the manufacturing of atidarsagene autotemcel therapy.(1)
Anti-Retrovirals/Elivaldogene Autotemcel
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: Elivaldogene autotemcel is prepared from apheresed cells that are transduced with a replication defective, self-inactivating lentiviral vector. Antiretrovirals may interfere with the manufacturing of apheresed cells.
CLINICAL EFFECTS: Use of antiretrovirals before mobilization and apheresis may interfere with the production of elivaldogene autotemcel.
PREDISPOSING FACTORS: None determined.
PATIENT MANAGEMENT: Discontinue antiretrovirals for at least one month prior to mobilization and until all cycles of apheresis are completed. If a patient requires antiretrovirals for HIV prophylaxis, then confirm a negative HIV test before beginning mobilization and apheresis of CD34+ cells.
DISCUSSION: Antiretroviral medications may interfere with the manufacturing of elivaldogene autotemcel therapy.(1)
Anti-Retrovirals/Etuvetidigene Autotemcel
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: Etuvetidigene autotemcel is prepared from apheresed cells that are transduced with a replication defective, self-inactivating HIV-based lentiviral vector. Antiretrovirals may interfere with the manufacturing of the apheresed cells.
CLINICAL EFFECTS: Use of antiretrovirals before mobilization and apheresis may interfere with the production of etuvetidigene autotemcel.(1)
PREDISPOSING FACTORS: None determined.
PATIENT MANAGEMENT: Patients should not take antiretrovirals for at least one month prior to mobilization and until at least 7 days after etuvetidigene autotemcel infusion.(1) If a patient requires antiretroviral agents for HIV post-exposure prophylaxis, etuvetidigene autotemcel treatment should be delayed until HIV testing is negative at 6 months post-exposure.(1)
DISCUSSION: Antiretroviral medications may interfere with the manufacturing of etuvetidigene autotemcel therapy.(1)
Anti-Retrovirals/Lovotibeglogene Autotemcel
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: Lovotibeglogene autotemcel is prepared from apheresed cells that are transduced with a replication defective, self-inactivating lentiviral vector. Antiretrovirals may interfere with the manufacturing of apheresed cells.
CLINICAL EFFECTS: Use of antiretrovirals before mobilization and apheresis may interfere with the production of lovotibeglogene autotemcel.(1)
PREDISPOSING FACTORS: None determined.
PATIENT MANAGEMENT: Discontinue antiretrovirals for at least one month prior to mobilization and until all cycles of apheresis are completed.(1) There are some long-acting antiretroviral medications that may require a longer duration of discontinuation for elimination of the medication. If a patient is taking anti-retrovirals for HIV prophylaxis, confirm a negative test for HIV before beginning mobilization and apheresis of CD34+ cells.(1)
DISCUSSION: Antiretroviral medications may interfere with the manufacturing of lovotibeglogene autotemcel therapy.(1)
Anti-Retrovirals; Hydroxyurea/Betibeglogene Autotemcel
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: Betibeglogene autotemcel is prepared from apheresed cells that are transduced with a replication defective, self-inactivating lentiviral vector. Antiretrovirals may interfere with the manufacturing of apheresed cells. Hydroxyurea may interfere with hematopoietic stem cell (HSC) mobilization of CD34+ cells.(1)
CLINICAL EFFECTS: Use of hydroxyurea before mobilization may result in unsuccessful stem cell mobilization. Use of antiretrovirals before mobilization and apheresis may interfere with the production of betibeglogene autotemcel.
PREDISPOSING FACTORS: None determined.
PATIENT MANAGEMENT: Discontinue antiretrovirals and hydroxyurea for at least one month prior to mobilization and until all cycles of apheresis are completed. If a patient requires antiretrovirals for HIV prophylaxis, then confirm a negative HIV test before beginning mobilization and apheresis of CD34+ cells.
DISCUSSION: Antiretroviral medications and hydroxyurea may interfere with the manufacturing of betibeglogene autotemcel therapy.(1)
Severe Interaction: Action is required to reduce the risk of severe adverse interaction.
Anti-Retrovirals/Marnetegragene Autotemcel
SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction.
MECHANISM OF ACTION: Marnetegragene autotemcel is prepared from apheresed cells that are transduced with a replication defective, self-inactivating lentiviral vector. Antiretrovirals may interfere with the manufacturing of transduced cells.
CLINICAL EFFECTS: Use of antiretrovirals before mobilization and apheresis may interfere with the production of marnetegragene autotemcel.
PREDISPOSING FACTORS: None determined.
PATIENT MANAGEMENT: Discontinue antiretrovirals for at least one month prior to mobilization (or the expected duration of time needed for elimination of the antiretrovirals) until all cycles of apheresis are completed. If a patient requires antiretrovirals for HIV prophylaxis, then confirm a negative HIV test before beginning mobilization and apheresis of CD34+ cells.(1)
DISCUSSION: Antiretroviral medications may interfere with the manufacturing of marnetegragene autotemcel.(1)
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)
Myelosuppressives; Immunomodulators/Sodium Iodide I 131
SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction.
MECHANISM OF ACTION: Sodium iodide I 131 can cause depression of the hematopoetic system. Myelosuppressives and immunomodulators also suppress the immune system.(1)
CLINICAL EFFECTS: Concurrent use of sodium iodide I 131 with agents that cause bone marrow depression, including myelosuppressives or immunomodulators, may result in an enhanced risk of hematologic disorders, including anemia, blood dyscrasias, bone marrow depression, leukopenia, and thrombocytopenia. Bone marrow depression may increase the risk of serious infections and bleeding.(1)
PREDISPOSING FACTORS: None determined.
PATIENT MANAGEMENT: The US manufacturer of sodium iodide I 131 states that concurrent use with bone marrow depressants may enhance the depression of the hematopoetic system caused by large doses of sodium iodide I 131.(1) Sodium iodide I 131 causes a dose-dependent bone marrow suppression, including neutropenia or thrombocytopenia, in the 3 to 5 weeks following administration. Patients may be at increased risk of infections or bleeding during this time. Monitor complete blood counts within one month of therapy. If results indicate leukopenia or thrombocytopenia, dosimetry should be used to determine a safe sodium iodide I 131 activity.(1)
DISCUSSION: Hematologic disorders including death have been reported with sodium iodide I 131. The most common hematologic disorders reported include anemia, blood dyscrasias, bone marrow depression, leukopenia, and thrombocytopenia.(1)
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
*Prior hypersensitivity reaction to ibalizumab or any components of the product.
- Lactation
There are no severe contraindications for this drug.
There are no moderate contraindications for this drug.
Adverse reactions
The most common adverse reactions (>=5%) include diarrhea, dizziness, nausea, and rash.
Less Frequent
- Neutropenic disorder
- Thrombocytopenic disorder
Rare or Very Rare
- Anaphylaxis
- Angioedema
- Dyspnea
More Frequent
- Diarrhea
- Dizziness
- Nausea
- Skin rash
Rare or Very Rare
- Chest tightness
- Cough
- Flushing
- Pruritus of skin
- Wheezing
Precautions
No enhanced messaging available.
Safety and efficacy of ibalizumab-uiyk have not been established in pediatric patients. The pharmacokinetics of the drug have not been evaluated in pediatric patients.
The Antiretroviral Pregnancy Registry (APR) monitors pregnancy outcomes in women exposed to antiretroviral medicines during pregnancy. Clinicians are encouraged to register patients in the APR by calling 800-258-4263.
There are no available data on ibalizumab use in pregnant women to evaluate for a drug-associated risk of major birth defects, miscarriage, or adverse maternal or fetal outcomes.
According to the 2023 HHS perinatal HIV treatment guideline, data are insufficient to make recommendations or characterize the risk of congenital anomalies with ibalizumab use during pregnancy.
Monoclonal antibodies, such as ibalizumab-, are transported across the placenta as pregnancy progresses. Based on animal data, ibalizumab use during pregnancy may cause reversible immunosuppression (CD4+ T cell and B cell lymphocytopenia) in infants exposed to ibalizumab-uiyk in utero. In a reproductive study in monkeys, reversible decreases in CD4+ T cells and B cells and increases in CD8+ T cells were observed within the first 4 weeks after birth in infants born to pregnant monkeys receiving ibalizumab-uiyk intravenously. Lymphocyte counts returned to near normal levels by 3 months of age. One infant monkey died from a systemic viral infection that may be related to ibalizumab-induced immunosuppression. No malformations or premature births were observed. If pregnancy occurs during ibalizumab treatment, refer to a specialist to provide guidance regarding monitoring and management (such as need for antibiotic or immunoprophylaxis) of exposed infants.
The safety of administering live or live-attenuated vaccines in exposed infants is unknown.
It is not known whether ibalizumab-uiyk is distributed into human milk, affects the breast-fed child, or affects milk production. Human IgG is distributed into milk in humans. However, data indicate that antibodies in breast milk do not enter the neonatal or infant circulatory system in substantial amounts.
The HHS perinatal HIV transmission guideline provides updated recommendations on infant feeding. The guideline states that patients with HIV should receive evidence-based, patient-centered counseling to support shared decision making about infant feeding. During counseling, patients should be informed that feeding with appropriate formula or pasteurized donor human milk from a milk bank eliminates the risk of postnatal HIV transmission to the infant. Additionally, achieving and maintaining viral suppression with antiretroviral therapy during pregnancy and postpartum reduces the risk of breastfeeding HIV transmission to <1%, but does not completely eliminate the risk. Replacement feeding with formula or banked pasteurized donor milk is recommended when patients with HIV are not on antiretroviral therapy and/or do not have a suppressed viral load during pregnancy (at a minimum throughout the third trimester), as well as at delivery.
The manufacturer makes no specific dosage recommendations for geriatric patients.
Ibalizumab-uiyk has not been studied in geriatric patients. The pharmacokinetics of the drug have not been evaluated in geriatric patients.
ICD codes
| Code | Type | Description |
|---|---|---|
| HIV infection | ||
| B20 | ICD10CM | Human immunodeficiency virus [HIv] disease |
| B97.35 | ICD10CM | Human immunodeficiency virus, type 2 [HIV 2] as the cause of diseases classified elsewhere |
| O98.7 | ICD10CM | Human immunodeficiency virus [HIv] disease complicating pregnancy, childbirth and the puerperium |
| O98.71 | ICD10CM | Human immunodeficiency virus [HIv] disease complicating pregnancy |
| O98.711 | ICD10CM | Human immunodeficiency virus [HIv] disease complicating pregnancy, first trimester |
| O98.712 | ICD10CM | Human immunodeficiency virus [HIv] disease complicating pregnancy, second trimester |
| O98.713 | ICD10CM | Human immunodeficiency virus [HIv] disease complicating pregnancy, third trimester |
| O98.719 | ICD10CM | Human immunodeficiency virus [HIv] disease complicating pregnancy, unspecified trimester |
| O98.72 | ICD10CM | Human immunodeficiency virus [HIv] disease complicating childbirth |
| O98.73 | ICD10CM | Human immunodeficiency virus [HIv] disease complicating the puerperium |
| Z21 | ICD10CM | Asymptomatic human immunodeficiency virus [HIv] infection status |
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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