Medical benefit pharmaceutical policies for providers
See the latest updates to our medical benefit pharmaceutical policies.
MBP 224.0 Tecartus (brexucabtagene autoleucel)
Tecartus (brexucabtagene autoleucel) is a CD19-directed genetically modified autologous T-cell immunotherapy in which a patient's T cells are reprogrammed with a transgene encoding a chimeric antigen receptor (CAR) to identify and eliminate CD19-expressing malignant and normal cells. The CAR is comprised of a murine single-chain antibody fragment which recognizes CD19 and is fused to CD28 and CD3 zeta. CD3 zeta is a critical component for initiating T-cell activation and antitumor activity. After binding to CD19-expressing cells, the CD28 and CD3-zeta costimulatory domains activate downstream signaling cascades, which results in T-cell activation, proliferation, acquisition of effector functions, and secretion of inflammatory cytokines and chemokines, leading to destruction of CD19-expressing cells. Brexucabtagene autoleucel is prepared from the patient's peripheral blood cells obtained via leukapheresis.
MBP 144.0 Tecentriq (atezolizumab)
Tecentriq (atezolizumab) is a humanized monoclonal antibody immune checkpoint inhibitor that binds to programmed death ligand 1 (PD-L1) to selectively prevent the interaction between the programmed cell death 1 (PD-1) and B7.1 (also known as CD80) receptors, while still allowing interaction between PD-L2 and PD-1. PD-L1 is an immune checkpoint protein expressed on tumor cells and tumor infiltrating cells and down regulates anti-tumor T-cell function by binding to PD-1 and B7.1; blocking PD-1 and B7.1 interactions restore antitumor T-cell function.
MBP 273.0 Tecvayli (teclistamab-cqyv)
Tecvayli (teclistamab-cqyv) is a humanized immunoglobulin G4-proline, alanine, alanine (IgG4-PAA) antibody, and bispecific B-cell maturation antigen (BCMA)-directed CD3 T-cell engager. Teclistamab binds to the CD3 receptor on the surface of T-cells, and BCMA expressed on the surface of multiple myeloma cells, which results in T-cell activation, the release of various proinflammatory cytokines, and the lysis of BCMA-expressing multiple myeloma cells.
New Policy 1/17/23
MBP 158.0 Tepadina (thiotepa)
Tepadina (thiotepa) is an alkylating agent that produces cross-linking of DNA strands leading to inhibition of DNA, RNA, and protein synthesis; thiotepa is cell-cycle independent.
MBP 217.0 Tepezza (teprotumumab-trbw)
Tepezza (teprotumumab-trbw) is an Insulin-Like Growth Factor-1 Receptor (IGF-1R) Antagonist, Monoclonal Antibody that binds to insulin-like growth factor-1 receptor inhibitor and blocks its activation and signaling. Teprotumumab's mechanism of action in patients with thyroid eye disease has not been fully characterized.
MBP 271.0 Terlivaz (terlipressin)
Terlivaz (terlipressin), a synthetic vasopressin analogue, has intrinsic activity; however, a majority of the activity results from conversion to lysine-vasopressin via slow enzymatic cleavage, producing an extended duration of systemic vasoconstriction. Reduces portal pressure and blood flow into portal vessels, increasing effective arterial blood volume and mean arterial pressure, thereby increasing blood flow to the kidneys.
New Policy 1/17/23
MBP 259.0 Tezspire (tezepelumab-ekko)
Tezspire (tezepelumab-ekko) is a human monoclonal antibody IgG2λ that binds to human thymic stromal lymphopoietin (TSLP), an epithelial cytokine, and prevents human TSLP from interacting with the heterodimeric TSLP receptor. Blocking TSLP with tezepelumab-ekko reduces biomarkers and cytokines associated with inflammation including blood eosinophils, airway submucosal eosinophils, IgE, FeNO, IL-5, and IL-13; however, the mechanism of tezepelumab-ekko action in asthma has not been definitively established.
MBP 246.0 Tivdak (tisotumab vedotin-tftv)
Tisotumab vedotin is a tissue factor (TF)-directed antibody drug conjugate (ADC) comprised of an anti-TF IgG1-kappa antibody conjugated to the microtubule-disrupting agent monomethyl auristatin E (MMAE), via a protease-cleavable valine-citrulline linker. The antibody is directed against cell surface TF, which is the primary initiator of the extrinsic blood coagulation cascade. Tisotumab vedotin’s anticancer activity is likely due to the ADC binding to TF expressing cancer cells, followed by internalization of the ADC-TF complex, and release of MMAE via proteolytic cleavage. MMAE disrupts the microtubule network of actively dividing cells, leading to cell cycle arrest and apoptosis. Tisotumab vedotin also mediates antibody-dependent cellular phagocytosis and antibody-dependent cellular cytotoxicity.
MBP 65.0 Torisel (temsirolimus)
Torisel (temsirolimus) is an mTOR kinase inhibitor. It is metabolized to sirolimus and suppresses the production of proteins that control progression through cell cycle and angiogenesis.
MBP 294.0 Trastuzumab (Herceptin) and Biosimilars
Trastuzumab is a monoclonal antibody which binds to the extracellular domain of the human epidermal growth factor receptor 2 protein (HER-2); it mediates antibody-dependent cellular cytotoxicity by inhibiting proliferation of cells which overexpress HER-2 protein.
New Policy 7/18/23
MBP 204.0 Triptodur (triptorelin)
Triptodur (triptorelin) is an agonist analog of gonadotropin releasing hormone (GnRH) and causes suppression of ovarian and testicular steroidogenesis due to decreased levels of LH and FSH with subsequent decrease in testosterone (male) and estrogen (female) levels. After chronic and continuous administration, usually 2 to 4 weeks after initiation, a sustained decrease in LH and FSH secretion occurs. When used for assisted reproductive technologies (ART), prevents premature LH surge in women undergoing controlled ovarian hyperstimulation.
MBP 172.0 Trisenox (arsenic trioxide)
Trisenox (arsenic trioxide) is an arsenical which induces apoptosis in APL cells via morphological changes and DNA fragmentation. It also damages or degrades the fusion protein promyelocytic leukemia (PML)-retinoic acid receptor (RAR) alpha
MBP 216.0 Trodelvy (sacituzumab govitecan-hziy)
Trodelvy (sacituzumab govitecan-hziy) is an antibody drug conjugate that consists of a humanized antitrophoblast cell-surface antigen 2 (Trop-2) monoclonal antibody coupled to the topoisomerase 1 inhibitor SN-38 via a cleavable linker (Bardia 2019). Trop-2 is overexpressed in many epithelial cancers and is associated with cancer cell growth; it has been detected in breast cancer cells (including triple-negative breast cancer cells). Sacituzumab govitecan binds to Trop-2 and is internalized; SN-38 is released in tumors both intracellularly and in the tumor microenvironment, leading to DNA damage, apoptosis, and cell death.
MBP 48.0 Truxima (rituximab-abbs)
Rituxan (rituximab), Truxima (rituximab-abbs), Ruxience (rituximab-pvvr), and Riabni (rituximab-arrx) are genetically engineered chimeric murine/human monoclonal antibodies directed against the CD20 antigen found on the surface of normal and malignant B lymphocytes. Rituximab has been shown to be effective in rheumatoid arthritis in three randomized controlled trials and is now FDA-approved for use in combination with methotrexate (MTX) for reducing signs and symptoms in adult patients with moderately- to severely-active rheumatoid arthritis (RA) who have had an inadequate response to one or more tumor necrosis factor (TNF) antagonist therapies.
MBP 57.0 Tysabri (natalizumab)
Tysabri (natalizumab) is a monoclonal antibody bioengineered from part of a mouse antibody to closely resemble a human antibody and binds to a protein called alpha-4-integrin. Integrins are found primarily on the surface of white blood cells which are thought to play a major role in causing the damage to the nervous system in multiple sclerosis (MS). Natalizumab blocks adhesion and subsequent migration of leukocytes into the gut by binding the α - 4 integrin thereby reducing chronic inflammation associated with Crohn’s disease.
MBP 283.0 Tzield (teplizumab-mzwv)
Tzield (teplizumab-mzwv) binds to CD3 (a cell surface antigen) on both CD4+ and CD8+ T cells, which leads to an increase in the proportion of regulatory T cells and of exhausted CD8+ T cells in peripheral blood. The mechanism behind the delay in progression from stage 2 to stage 3 type 1 diabetes mellitus may involve partial agonistic signaling and deactivation of pancreatic beta cell autoreactive T lymphocytes.
New Policy 5/16/23
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