Commercial

Medical Policy

Title:

Betibeglogene Autotemcel [Beti-Cel (ZYNTEGLO®)]

Policy #:

08.01.89a

Policy

MEDICALLY NECESSARY

Betibeglogene autotemcel [Beti-Cel (Zynteglo®)] is considered medically necessary and, therefore, covered for the treatment of individuals with β-thalassemia who require regular peripheral blood transfusions to maintain target hemoglobin levels when prescribed by or in consultation with a hematologist when ALL of the following criteria are also met:

Individual has genetically confirmed diagnosis of β-thalassemia

Individual meets one of the following:

Age ≥5 years and ≤50 years
If age <5 years, individual meets both of the following:

Weight ≥6 kg

Provider submits medical rationale that individual is anticipated to be able to provide at least the minimum number of cells required to initiate the manufacturing process

Individual has a Karnofsky performance status (PS) of ≥80 for adults (≥16 years of age) or a Lansky PS of ≥80 for adolescents (<16 years of age)

Individual has a clinical diagnosis of transfusion-dependent β-thalassemia (β-thalassemia major or TDT), and has documentation of one of the following in the 2 previous years

Receipt of ≥8 transfusions of packed red blood cells (pRBC) per year

Receipt of ≥100 mL/kg pRBC per year

Individual is eligible for an allogeneic hematopoietic stem cell transplantation (HSCT)

Individual has not received prior allogeneic HSCT or gene therapy

Individual does not have any of the following:

Availability of human leukocyte antigen–identical or human leukocyte antigen–matched donor
T2*-weighted magnetic resonance imaging measurement of myocardial iron of less than 10 msec or other evidence of severe iron overload in the opinion of treating physician
Advanced liver disease (meets any one of the following)

Persistent aspartate transaminase, alanine transaminase, or direct bilirubin value greater than three times the upper limit of normal

Baseline prothrombin time or partial thromboplastin time greater than 1.5 times the upper limit of normal

Magnetic resonance imaging of the liver demonstrating clear evidence of cirrhosis

Liver biopsy demonstrating cirrhosis, any evidence of bridging fibrosis, or active hepatitis

Baseline estimated glomerular filtration rate less than 70 mL/min/1.73 m²
History of receiving prior gene therapy or allogeneic hematopoietic stem cell transplant
Any prior or current malignancy (with the exception of adequately treated cone-biopsied in situ carcinoma of the cervix uteri and basal or squamous cell carcinoma of the skin) or myeloproliferative or significant immunodeficiency disorder
Any immediate family member (i.e., parent or siblings) with a known familial cancer syndrome (including but not limited to hereditary breast and ovarian cancer syndrome, hereditary nonpolyposis colorectal cancer syndrome and familial adenomatous polyposis)
Active, uncontrolled hepatitis C virus or hepatitis B virus infection
Contraindication to the use of granulocyte colony stimulating factor (G-CSF), plerixafor, busulfan, or any other medicinal products required during myeloablative conditioning, including hypersensitivity to the active substances or to any of the excipients
A white blood cell count less than 3 × 10⁹/L, and/or platelet count less than 100 × 10⁹/L not related to hypersplenism

NOTE: Evio has been selected by the Company to administer clinical outcomes monitoring for individuals receiving certain high-cost drug therapies. Betibeglogene autotemcel [Beti-Cel (Zynteglo)] is included in the portfolio of high-cost drug/biologic therapies for which Evio will be tracking clinical outcomes. If an individual meets all medical policy criteria, the requesting physician and/or individual being treated must agree to providing clinical outcomes data and information via Evio's secure web portal as requested.

EXPERIMENTAL/INVESTIGATIONAL

All other uses for betibeglogene autotemcel [Beti-Cel (Zynteglo)], including any re-treatment with this therapy, are considered experimental/investigational and, therefore, not covered unless the indication is supported as an accepted off-label use, as defined in the Company medical policy on off-label coverage for prescription drugs and biologics.

REQUIRED DOCUMENTATION

The individual's medical record must reflect the medical necessity for the care provided. These medical records may include, but are not limited to, records from the professional provider's office, hospital, nursing home, home health agencies, therapies, and test reports.

The Company may conduct reviews and audits of services to our members, regardless of the participation status of the provider. All documentation is to be available to the Company upon request. Failure to produce the requested information may result in a denial for the drug.

Guidelines

β-Thalassemia Genotype Examples:

β⁰/β⁰
β⁰/β⁺
β⁺ IVS1-110/β⁺ IVS1-110
β^E/β⁰

Different Types of β-Thalassemia

Type	Genotype	Description
β-thalassemia major (generally transfusion dependent)	β⁰/β⁰ or β⁰/β⁺	Presents within the first 2 years of life with severe microcytic anemia (typical hemoglobin, 3–4 g/dL), mild jaundice, and hepatosplenomegaly Requires regular red blood cell transfusions and other medical treatments
Thalassemia intermedia	β⁺/β⁺	Presents at a later age with similar, but milder, clinical signs and symptoms of thalassemia Moderately severe anemia; some may need regular blood transfusion
Thalassemia minor	β/β⁰ or β/β⁺	Also called “β-thalassemia carrier" or “β-thalassemia trait" Usually clinically asymptomatic but may have a mild anemia Generally do not require any treatment

β⁰ refers to no β-globin production; β⁺ refers to decreased β-globin production.

Conversion of red blood cell (RBC) units from mL: 1 RBC unit in these criteria refer to a quantity of packed RBC (pRBC) approximately 200–350 mL.

Sites that use transfusion bags within this range, or ≥350 mL, the conversion in units should be done by dividing the volume transfused to the patient by 350 mL.
Sites that use transfusion bags <200 mL, the conversion in units should be done by dividing the volume transfused to the patient by 200 mL.

Examples of advanced liver disease include, but are not limited to, the following:

Cirrhosis
Active hepatitis
Bridging fibrosis
Fatty liver disease

BENEFIT APPLICATION

Subject to the terms and conditions of the applicable benefit contract, Betibeglogene Autotemcel [Beti-Cel (Zynteglo®)] is covered under the medical benefits of the Company’s products when the medical necessity criteria listed in this medical policy are met.

US FOOD AND DRUG ADMINISTRATION (FDA) STATUS

Betibeglogene autotemcel [Beti-Cel (Zynteglo®)] received approval from the U.S. Food and Drug Administration (FDA) on 08/17/2022. Per the FDA, Zynteglo® is an autologous hematopoietic stem cell–based gene therapy indicated for the treatment of adult and pediatric patients with β-thalassemia who require regular RBC transfusions.

Description

β-THALASSEMIA

β-thalassemia is an inherited blood disorder caused by a genetic mutation of the HBB gene that leads to reduced or absent synthesis of the β-globin proteins of hemoglobin (components of red blood cells [RBCs] responsible for carrying oxygen). Markedly reduced or absent β-globin leads to ineffective production and increased destruction of RBCs, manifesting in clinically significant anemia.

β-Thalassemia is an autosomal recessive disorder. Individuals who carry a mutation in only one copy of the HBB gene are generally asymptomatic or only have mild anemia (β-thalassemia minor or trait, hemoglobin [Hb] >10.0 g/dL). It is estimated that 1.5% of the global population carries at least one defective copy of the HBB gene, with certain geographic areas having a higher local prevalence—primarily in the Mediterranean, Africa, the Middle East, and South Asia. However, if both copies of the HBB gene have a mutation, there will be a reduction or absence of β-globin. The degree to which β-globin is reduced depends on the specific mutation and how many genes are affected: β⁰/β⁰ (completely absent β-globin), β⁺/β⁺ (some β-globin production; severity depends on mutation), or β⁺/β⁰ (one gene copy produces some β-globin, the other produces none). Individuals with completely absent β-globin have a more severe clinical course, typically presenting in the first 6 to 24 months of life, with severe anemia, failure to thrive, and end-organ damage; prompt initiation of transfusion therapy is required to prevent early mortality. Conversely, individuals with some β-globin production have variable clinical presentations, with some individuals depending on routine transfusions to maintain health and quality of life, whereas others might have mild symptoms or only receive transfusions in times of stress (e.g., pregnancy, infection, surgery). Historically, individuals with absent β-globin were considered to have thalassemia major and those with reduced β-globin were considered to have thalassemia intermedia, but it is clinically preferable to classify thalassemia based on clinical severity and transfusion requirements regardless of the underlying genotype. The 2021 guidelines published by the Thalassaemia International Federation (TIF) classify β-thalassemia phenotypically into two main groups: transfusion-dependent thalassemia (TDT) and non–transfusion-dependent thalassemia (NTDT).

β-Thalassemias are usually caused by point mutations in or near the β-globin gene on chromosome 11. The mutations may affect the gene promoter sequence, the 5' untranslated sequence (UTR) of the coding region, the initiation codon; or the mutations may involve RNA processing, leading to inefficient or absent splicing. β⁺ mutations result in a reduced (but not absent) rate of synthesis of β-polypeptide chains and range from severe to mild, whereas in β⁰ mutations, there is no detectable β-globin production from the mutated allele.

β-Thalassemia traits refer to either the β/β⁺ or the β/β⁰ genotype. These are clinically mild conditions that result in microcytosis, mild anemia, and an elevated RBC count. The β-thalassemia homozygote or compound heterozygote state results in a more severe phenotype. The β⁰/β⁰, β⁺/β⁺, or β⁺/β⁰ state, in which the β-plus (β⁺) mutation is severe, will produce a TDT major; the β⁺/β⁺ genotype involving the milder β mutations may produce a thalassemia intermedia.

The diagnostic hallmark of the β-thalassemia trait on hemoglobin analysis is an elevated relative percentage of hemoglobin (Hb) A2. In this condition, the Hb A2 is typically 4% to 8%, with a mean of about 5% to 6%. However, elevation of Hb A2 is not universal in all β-thalassemia traits. A notable exception is β-thalassemia with coexistent iron deficiency, in which iron deficiency may suppress or mask the Hb A2 elevation, so the percentage Hb A2 is best judged following iron repletion. There may also be a slight elevation of Hb F in β-thalassemia traits. This elevation is not usually more than 5% to 7% of the total hemoglobin.

β-Thalassemia homozygotes or compound heterozygotes have a more marked anemia in which Hb F may be the dominant hemoglobin. The relative percentage of adult Hb A varies from 0% in the β⁰/β⁰ state to over 30% in milder β⁺/β⁺ variants.

Lifelong, regular blood transfusions and removal of excess iron through chelation are the mainstays of treatment for patients with TDT. Routine transfusions, typically every 2 to 5 weeks, aim to keep hemoglobin at a level that suppresses the body's production of its own (abnormal) hemoglobin. However, as excess iron accumulates as a consequence of repeated transfusion and increased gut absorption, chelation is critical for treating and preventing complications from iron overload (e.g., pulmonary hypertension, liver dysfunction, cardiac manifestations)—the main source of morbidity and mortality in TDT. In addition, individuals with TDT also contend with other disease-related complications such as problems with growth and development, diabetes and other endocrine abnormalities, and fertility and pregnancy-related concerns. There is also the ongoing risk of transfusion-related side effects and infections, although the latter are rare with modern blood-screening procedures. Standard of care may also include treatment with luspatercept-aamt (Reblozyl®, Acceleron Pharma Inc. and Bristol Myers Squibb/Celgene Corp.), a biologic that can enhance erythropoietic maturation and differentiation resulting in increased RBC production, thereby reducing transfusion burden in some individuals.

Hematopoietic stem cell transplantation (HSCT) is currently the only curative treatment for TDT. Ideally, HSCT is performed in children younger than 14 years of age with a human leukocyte antigen (HLA)–matched sibling donor. In such candidates, the cure rate is over 90% with a 4% risk of mortality. The cure rate decreases in older patients, those with extensive iron toxicity, and those without a matched donor. Lack of compatible donors is a central limitation of initiating HSCT; not more than 25% of patients have access to compatible related or unrelated donors.

BETIBEGLOGENE AUTOTEMCEL (BETI-CEL [ZYNTEGLO®])

Betibeglogene autotemcel (Beti-cel), marketed under the brand name Zynteglo, is an emerging, potentially curative gene therapy for β-thalassemia. Betibeglogene autotemcel (Beti-cel [Zynteglo]) uses a lentivirus vector to insert a functioning version of the HBB gene into the individual's own blood cells. This is accomplished by retrieving stem cells from the individual's blood, engineering them outside of the body, and then transplanting cells with functioning HBB genes back into the body. The individual must receive chemotherapy to prepare the bone marrow to receive the modified cells and to produce new red cells with normal β-globin/hemoglobin. This product received approval from the US Food and Drug Administration (FDA) on August 17, 2022. Per the FDA, Zynteglo is an autologous hematopoietic stem cell–based gene therapy indicated for the treatment of adult and pediatric patients with β-thalassemia who require regular RBC transfusions.

Beti-Cel (Zynteglo) gene therapy for transfusion-dependent β-thalassemia contains autologous CD34+ hematopoietic stem cells and progenitor cells transduced with the BB305 lentiviral vector encoding the β-globin (βA-T87Q) gene.

An open-label, phase III study (HGB-207 [Northstar-2]) evaluated the efficacy and safety of betibeglogene autotemcel (Beti-Cel [Zynteglo]) in adult and pediatric individuals with transfusion-dependent β-thalassemia and a non–β⁰/β⁰ genotype. Individuals underwent myeloablation with busulfan (with doses adjusted on the basis of pharmacokinetic analysis) and received (Beti-Cel [Zynteglo]) intravenously. The primary endpoint for this study, reported by Locatelli et al. (2021), was transfusion independence (i.e., a weighted average hemoglobin level of ≥9 g/dL without red cell transfusions for ≥12 months).

Peer-reviewed published results from Locatelli et al. (2021) stated that 23 individuals were enrolled and received treatment, with a median follow-up of 29.5 months (range, 13.0–48.2). Transfusion independence occurred in 20 of 22 patients who could be evaluated (91%), including six of seven patients (86%) who were younger than 12 years of age. The average hemoglobin level during transfusion independence was 11.7 g/dL (range, 9.5–12.8). Twelve months after Beti-cel infusion, the median level of gene therapy–derived adult hemoglobin (HbA) with a T87Q amino acid substitution (HbAT87Q) was 8.7 g/dL (range, 5.2–10.6) in patients who had transfusion independence. The safety profile of Beti-cel was consistent with that of busulfan-based myeloablation. Four individuals had at least one adverse event that was considered by the investigators to be related or possibly related to Beti-cel; all events were nonserious except for thrombocytopenia (in one patient). No cases of cancer were observed.

The authors concluded that treatment with Beti-cel resulted in a sustained HbAT87Q level and a total hemoglobin level that was high enough to enable transfusion independence in most patients with a non-β⁰/β⁰ genotype, including those younger than 12 years of age (funded by Bluebird Bio; HGB-207 ClinicalTrials.gov number NCT02906202). The phase III HGB-212 (Northstar-3) study (NCT03207009) is underway to evaluate patients with the β⁰/β⁰, β⁰/β⁺IVS-I-110, and β⁺IVS-I-110/β⁺IVS-I-110 genotypes.

SUMMARY

β-thalassemia is a genetic hemoglobinopathy that results from defects in β-globin synthesis leading to reduced synthesis or absence of β-globin chains causing impaired production of hemoglobin. The clinical presentation is that of anemia, which requires transfusion and multiple downstream sequelae from iron overload. It is estimated that at least 1000 people in the United States have transfusion-dependent β-thalassemia. Betibeglogene autotemcel contains autologous CD34+ hematopoietic stem cells in which functional copies of a modified form of the β-globin gene (βA-T87Q-globin gene) have been added. Once the hematopoietic stem cells reengineered with βA-T87Q are infused, they engraft in the bone marrow and differentiate to produce RBCs containing βA-T87Q gene that will produce HbAT87Q protein (functional gene therapy–derived hemoglobin) at levels that may eliminate or significantly reduce the need for transfusions.

For individuals with transfusion-dependent β-thalassemia who receive betibeglogene autotemcel (Beti-Cel [Zynteglo]), the evidence includes two single-arm studies: HGB-207 (Northstar-2) and HGB-212 (Northstar-3 [underway and ongoing]). The Northstar-2 trial enrolled non-β⁰β⁰ genotype (less-severe phenotype relative to β0β0 genotype), whereas the Northstar-3 trial enrolled β-thalassemia patients with either a β⁰or β⁺ IVS1 110 (G>A) variant (severe phenotype) at both alleles of the HBB gene. Relevant outcomes are change in disease status, quality of life, hospitalizations, medication use, treatment-related morbidity, and treatment-related mortality. The two open-label, phase III, single-arm studies included a total of 41 individuals who received a single intravenous infusion of betibeglogene autotemcel (Beti-Cel [Zynteglo]). Of the 41 participants, 36 participants in whom transfusion independence was evaluable were included in the efficacy analysis. Transfusion independence was achieved in 89% (95% confidence interval [CI], 74%–97%) of study participants. Limitations include a small sample size and limited duration of follow-up. There is uncertainty regarding the durability of effect over a longer time period. Long-term follow-up (>15 years) is required to establish precision around durability of the treatment effect. The small sample size creates uncertainty around the estimates of some of the patient-important outcomes, particularly adverse events. Some serious harms are likely rare occurrences and, as such, may not be observed in small trials. Although most of the serious adverse events were attributable to known risks associated with myeloablative conditioning, uncertainty still remains about the degree of risk with betibeglogene autotemcel (Beti-Cel [Zynteglo]) infusion in real-world practice. Insertional oncogenesis has been identified as a potential risk with transgene integration. There has been no evidence of insertional oncogenesis and no malignancies in the trials of betibeglogene autotemcel (Beti-Cel [Zynteglo]). However, cases of myelodysplastic syndrome and acute myeloid leukemia have been reported in gene therapy trials that use a lentiviral vector to treat other conditions. The evidence is sufficient to determine that the technology results in an improvement in the net health outcome in severest cases of TDT within select subpopulations of β-thalassemia major, as elicited and derived by the genotypes of Northstar-3, a sizeable number of severe genotypes in Northstar-2, and parameters for transfusion dependence in these and only available clinical investigations.

References

Angelucci E, Matthes-Martin S, Baronciani D, et al. Hematopoietic stem cell transplantation in thalassemia major and sickle cell disease: indications and management recommendations from an international expert panel. Haematologica. 2014;99(5):811-820.

Arian M, Mirmohammadkhani M, Ghorbani R, et al. Health-related quality of life (HRQoL) in beta-thalassemia major (β-TM) patients assessed by 36-item short form health survey (SF-36): a meta-analysis. Qual Life Res. 2019;28(2):321-334.

Baronciani D, Angelucci E, Potschger U, et al. Hemopoietic stem cell transplantation in thalassemia: a report from the European Society for Blood and Bone Marrow Transplantation Hemoglobinopathy Registry, 2000-2010. Bone Marrow Transplant. 2016;51(4):536-541.

Beaudoin FL, Richardson M, Synnott PG, et al. Betibeglogene Autotemcel for Beta Thalassemia: Effectiveness and Value; Final Evidence Report. Institute for Clinical and Economic Review, July 19, 2022. https://icer.org/beta-thalassemia-2022/#timeline beta-thalassemia (beta-thal). Bluebird Bio. https://www.bluebirdbio.com/our-focus/transfusion-dependant-beta-thalassemia. Accessed July 15, 2022.

Borgna-Pignatti C. The life of patients with thalassemia major. Haematologica. 2010;95(3):345-348.

Caocci G, Orofino MG, Vacca A, et al. Long-term survival of beta thalassemia major patients treated with hematopoietic stem cell transplantation compared with survival with conventional treatment. Am J Hematol. 2017;92(12):1303-1310.

Cappellini MD, Cohen A, Porter J, et al., editors. Guidelines for the Management of Transfusion Dependent Thalassaemia (TDT) [Internet]. 3rd edition. Nicosia (CY): Thalassaemia International Federation; 2014.

Cazzola M, Borgna-Pignatti C, Locatelli F, et al. A moderate transfusion regimen may reduce iron loading in beta-thalassemia major without producing excessive expansion of erythropoiesis. Transfusion. 1997;37(2):135-140.

Cazzola M, Locatelli F, De Stefano P. Deferoxamine in thalassemia major. N Engl J Med. 1995;332(4):271-2; author reply 272-273.

Chieco P, Butler C. 2021 CAF Information - The Cooley's Anemia Foundation. Published January 21st, 2022. Available at: https://www.thalassemia.org/2021-caf-information/. Accessed Aug 3, 2022.

Chonat S, Quinn CT. Current standards of care and long term outcomes for thalassemia and sickle cell disease. Adv Exp Med Biol. 2017;1013:59-87.

ClinicalTrials.gov. A study evaluating the efficacy and safety of the Lentiglobin® BB305 drug product in subjects with transfusion-dependent β-thalassemia, who do not have a β0/β0 genotype. Last updated June 25, 2021. Available at: https://clinicaltrials.gov/ct2/show/NCT02906202. Accessed June 26, 2021.

ClinicalTrials.gov. A study evaluating the efficacy and safety of the Lentiglobin® BB305 drug product in subjects with transfusion-dependent β-thalassemia. Last updated June 24, 2021. Available at: https://classic.clinicaltrials.gov/ct2/show/NCT03207009. Accessed June 26, 2021.

Dimitrios et al. 2021 Thalassaemia International Federation Guidelines for the Management of Transfusion-dependent Thalassemia. HemaSphere. 2022;6(8):e732.

Galanello R, Origa R. Beta-thalassemia. Orphanet J Rare Dis. 2010;5:11.

Institute for Clinical and Evidence Review. Betibeglogene Autotemcel for Beta Thalassemia: Effectiveness and Value (Final Evidence Report July 19, 2022). Available at: https://icer.org/beta-thalassemia-2022. Accessed August 4, 2022.

Kremastinos DT, Farmakis D, Aessopos A, et al. Beta-thalassemia cardiomyopathy: history, present considerations, and future perspectives. Circ Heart Fail. 2010;3(3):451-458.

Locatelli F, Thompson AA, Kwiatkowski JL, et al. Betibeglogene autotemcel gene therapy for non-β⁰/β⁰ genotype β-thalassemia. N Engl J Med. 2022;386(5):415-427.

Magrin E, Semeraro M, Hebert N, et al. Long-term outcomes of lentiviral gene therapy for the β-hemoglobinopathies: the HGB-205 trial. Nat Med. 2022;28(1):81-88.

Olivieri NF, Liu PP, Sher GD, et al. Brief report: combined liver and heart transplantation for end-stage iron-induced organ failure in an adult with homozygous beta-thalassemia. N Engl J Med. 1994;330(16):1125-1127.

Origa R. Beta-Thalassemia. 2000 Sep 28 [Updated 2021 Feb 4]. In: Adam MP, Mirzaa GM, Pagon RA, et al., editors. GeneReviews [Internet]. Seattle (WA): University of Washington, Seattle; 1993-2022. Available at: https://www.ncbi.nlm.nih.gov/books/NBK1426/.

Porter JB, Thompson AA, Walters MC, et al. Improvement in erythropoiesis in patients with transfusion dependent β-thalassemia following treatment with betibeglogene autotemcel (LentiGlobin for β-thalassemia) in the phase 3 Hgb-207 study. EHA 2020 Virtual Congress Abstract: S296.

Prescribing Label: ZYNTEGLO (betibeglogene autotemcel) suspension for intravenous infusion. Initial U.S. Approval: 2022. Available at: https://www.fda.gov/media/160991/download. Accessed Aug 17, 2022.

Sharma A, Jagannath VA, Puri L. Hematopoietic stem cell transplantation for people with β-thalassaemia. Cochrane Database Syst Rev. 2021;4:CD008708.

Standards of Care Guidelines for Thalassemia: 2012. Oakland, CA: Childrens Hospital & Research Center Oakland. Available at: https://thalassemia.com/documents/SOCGuidelines2012.pdf. Accessed August 4, 2022.

Thompson AA, Cunningham MJ, Singer ST, et al. Red cell alloimmunization in a diverse population of transfused patients with thalassaemia. Br J Haematol. 2011;153(1):121-128.

Thompson AA, Walters MC, Kwiatkowski J, et al. Gene therapy in patients with transfusion-dependent β-thalassemia. N Engl J Med. 2018;378(16):1479-1493.

Trachtenberg F, Vichinsky E, Haines D, et al. Iron chelation adherence to deferoxamine and deferasirox in thalassemia. Am J Hematol. 2011;86(5):433-436.

Vitrano A, Calvaruso G, Lai E, et al. The era of comparable life expectancy between thalassaemia major and intermedia: Is it time to revisit the major-intermedia dichotomy? Br J Haematol. 2017;176(1):124-130.

Coding

CPT Procedure Code Number(s)

N/A

ICD - 10 Procedure Code Number(s)

N/A

ICD - 10 Diagnosis Code Number(s)

THE FOLLOWING CODE REPRESENTs TRANSFUSION DEPENDENT β-THALASSEMIA TYPES; BETA THALASSEMIA MAJOR, HOMOZYGOUS BETA THALASSEMIA AND SEVERE BETA THALASSEMIA:

D56.1 Beta thalassemia

HCPCS Level II Code Number(s)

J3393 Injection, betibeglogene autotemcel, per treatment

Revenue Code Number(s)

N/A

MPMiscCodesNarrativesPub

Coding and Billing Requirements

Cross Reference

Policy History

Version Effective Date:

7/1/2024

Version Issued Date: