Current medical benefit pharmaceutical policies
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MBP 235.0 Abecma (idecabtagene vicleucel)
Abecma (idecabtagene vicleucel) is a B-cell maturation antigen (BCMA)-directed genetically modified autologous T-cell immunotherapy in which a patient’s T-cells are reprogrammed with an anti-BCMA02 chimeric antigen receptor (CAR) lentiviral vector. The CAR construct includes an anti-BCMA single chain variable fragment-targeting domain for antigen specificity, a transmembrane domain, a CD3-zeta T-cell activation domain, and a 4-1BB costimulatory domain. CD3-zeta signaling initiates activation and antitumor activity, while 4-1BB (CD137) signaling enhances T-cell expansion. Antigen-specific activation of idecabtagene vicleucel results in CAR-positive T-cell proliferation, cytokine secretion, and subsequent cytolytic killing of BCMA-expressing cells. Idecabtagene vicleucel is prepared from the patient's T-cells, which are obtained via leukapheresis.
MBP 36.0 Abraxane (paclitaxel protein bound particles)
Abraxane (paclitaxel protein bound particles) is a formulation of paclitaxel that is free of the solvent polyoxyethylated castor oil (Cremophor), which is thought to be the cause of the hypersensitivity reactions frequently encountered with standard paclitaxel.
MBP 76.0 Actemra IV (tocilizumab)
Actemra IV (tocilizumab) is a humanized interleukin-6 receptor–inhibiting monoclonal antibody. It competes for both membrane-bound and soluble forms of the human interleukin-6 receptor, thus inhibiting the binding of interleukin to its receptors and leading to the blockade of interleukin-6 signaling through the soluble and membrane-bound interleukin-6 receptors. Interleukin-6 is a pro-inflammatory cytokine commonly expressed in patients with rheumatoid arthritis.
MBP 212.0 Adakveo (crizanlizumab-tmca)
Adakveo (crizanlizumab-tmca) is a humanized monoclonal antibody, which binds to P-selectin and blocks interaction with ligands, including P-selectin glycoprotein ligand 1. Normally, the translocation of P-selectin to the activated endothelial cell surface results in adhesion of sickle erythrocytes to vessels and the development of vascular occlusion. By binding to P-selectin, Adakveo inhibits interactions between endothelial cells, platelets, red blood cells, and leukocytes, which results in decreased platelet aggregation, maintenance of blood flow, and minimized sickle cell-related crises.
MBP 166.0 Adcetris (brentuximab vedotin)
Adcetris (brentuximab vedotin) is an antibody drug conjugate (ADC) directed at CD30 consisting of 3 components: 1) a CD30-specific chimeric IgG1 antibody cAC10; 2) a microtubule-disrupting agent, monomethylauristatin E (MMAE); and 3) a protease cleavable dipeptide linker (which covalently conjugates MMAE to cAC10). The conjugate binds to cells which express CD30, and forms a complex which is internalized within the cell and releases MMAE. MMAE binds to the tubules and disrupts the cellular microtubule network, inducing cell cycle arrest (G2/M phase) and apoptosis.
MBP 192.0 Akynzeo IV (fosnetupitant/palonosetron)
Akynzeo IV (fosnetupitant/palonosetron) is a selective 5-HT3 receptor antagonist and substance P/neurokinin 1 receptor antagonist combination. Fosnetupitant is a prodrug of netupitant, a selective substance P/neurokinin (NK1) receptor antagonist, which augments the antiemetic activity of 5-HT3 receptor antagonists and corticosteroids to inhibit acute and delayed chemotherapy-induced emesis. Palonosetron is a selective 5-HT3 receptor antagonist, which blocks serotonin, both on vagal nerve terminals in the periphery and centrally in the chemoreceptor trigger zone. Palonosetron inhibits the cross-talk between the 5-HT3 and NK1 receptors. The combination of palonosetron and netupitant works synergistically to inhibit substance P response to a greater extent than either agent alone
MBP 7.0 Aldurazyme (laronidase)
Aldurazyme (laronidase) is used to treat mucopolysaccaridosis I (MPS I), an autosomal recessive disorder which causes a deficiency of alpha-L-iduronidase, an enzyme required to break down glycosaminoglycans.
MBP 161.0 Aliqopa (copanlisib)
Aliqopa (copanlisib) inhibits phosphatidylinositol 3-kinase (PI3K), primarily the P13K-alpha and P13K-delta isoforms which are expressed in malignant B-cells. Copanlisib induces tumor cell death through apoptosis and inhibition of proliferation of primary malignant B cell lines. In addition, copanlisib inhibits several signaling pathways, including B-cell receptor signaling, CXCR12 mediated chemotaxis of malignant B cells and NFκB signaling in lymphoma cell lines.
MBP 24.0 Aloxi (palonosetron)
Aloxi (Palonosetron) is a 5-HT3 antagonist indicated for the prevention of chemotherapy induced nausea and vomiting.
MBP 43.0 Alpha 1-Antitrypsin Inhibitor Therapy (Prolastin-C, Aralast, Zemaira, Glassia)
Alpha 1-antitrypsin (AAT) deficiency is an autosomal co-dominant genetic condition that may predispose people with the condition to emphysema in adult life, and liver disease in adults and children. In rare cases, alpha-1 antitrypsin deficiency also causes a skin condition characterized by hardened skin with painful lumps or patches.
MBP 149.0 Ameluz (aminolevulinic acid)
Ameluz (aminolevulinic acid) is a metabolic precursor of the photosensitizer protoporphyrin IX (PpIX). Photosensitization following local/topical application of aminolevulinic acid occurs through the metabolic conversion to PpIX. When exposed to light of appropriate wavelength and energy, accumulated PpIX produces a photodynamic reaction resulting in local cytotoxicity. Precancerous and cancerous cells exhibit a higher rate of porphyrin induction compared to normal cells.
MBP 241.0 Amondys 45 (casimersen)
Casimersen is an antisense oligonucleotide designed to bind exon 45 of dystrophin pre-mRNA, resulting in exclusion of this exon during mRNA processing. Skipping of exon 45 allows for production of an internally truncated dystrophin protein in patients with a confirmed mutation that is amenable to exon 45 skipping.
MBP 268.0 Amvuttra (vutrisiran)
Amvuttra (vutrisiran) is a double-stranded small interfering ribonucleic acid (siRNA)-N-acetylgalactosamine (GalNAc) conjugate that causes degradation of mutant and wild-type transthyretin (TTR) messenger RNA (mRNA) through RNA interference, which results in a reduction of serum TTR protein and TTR protein deposits in tissues.
MBP 183.0 Andexxa (andexanet alfa)
Andexxa (andexanet alfa) is an antidote that binds and sequesters the FXa inhibitors Xarelto (rivaroxaban) and Eliquis (apixaban). In addition, andexanet alfa inhibits the activity of Tissue Factor Pathway Inhibitor (TFPI), increasing tissue factor-initiated thrombin generation.
MBP 261.0 Anjeso (meloxicam injection)
Anjeso (meloxicam injection) is an intravenous formulation of meloxicam. Meloxicam reversibly inhibits cyclooxygenase-1 and 2 (COX-1 and 2) enzymes, which results in decreased formation of prostaglandin precursors; has antipyretic, analgesic, and anti-inflammatory properties. Other proposed mechanisms not fully elucidated (and possibly contributing to the anti-inflammatory effect to varying degrees), include inhibiting chemotaxis, altering lymphocyte activity, inhibiting neutrophil aggregation/activation, and decreasing proinflammatory cytokine levels.
New Policy 6/24/22
MBP 64.0 Arranon (nelarabine)
Arranon (nelarabine) is a pro-drug of the cytotoxic deoxyguanosine analogue, 9-β-D-arabinofuranosylguanine (ara-G). Nelarabine is demethylated by adenosine deaminase (ADA) to ara-G, mono-phosphorylated by deoxyguanosine kinase and deoxycytidine kinase, and subsequently converted to the active 5’-triphosphate, ara-GTP. Accumulation of ara-GTP in leukemic blasts allows for incorporation into deoxyribonucleic acid (DNA), leading to inhibition of DNA synthesis and cell death.
MBP 73.0 Arzerra (ofatumumab)
Arzerra (ofatumumab) is a monoclonal antibody that binds to a specific protein found on the surface of both normal and malignant B cells, making the cells more susceptible to immune system attack.
MBP 116.0 Aveed (testosterone undecanoate)
Aveed (testosterone undecanoate) injection is an androgen indicated for testosterone replacement therapy in adult males for conditions associated with a deficiency or absence of endogenous testosterone.
MBP 5.0 Avsola (infliximab-axxq) or Remicade (infliximab) or Inflectra (infliximab-dyyb) or Renflexis (infliximab-abda)
Infliximab is a therapeutic agent that inhibits activity of tumor necrosis factor alpha (TNF-alpha), a biological response mediator of inflammation. TNF-alpha is a key inflammatory mediator in rheumatoid arthritis, Crohn’s disease and other autoimmune disorders. In these chronic conditions, overproduction of TNF-alpha leads to inflammation. Infliximab reduces inflammation by binding to and neutralizing TNF- alpha on the cell membrane and in the blood. Infliximab-dyyb, infliximab-abda, and infliximab-axxq are biosimilar agents of Infliximab.
MBP 132.0 Avycaz (cetfazidime/avibactam)
Avycaz (cetfazidime/avibactam) is a combination cephalosporin/beta-lactamase inhibitor indicated in combination with metronidazole, for the treatment of complicated intra-abdominal infections (cIAI) caused by the following susceptible microorganisms: Escherichia coli, Klebsiella pneumoniae, Proteus mirabilis, Enterobacter cloacae, Klebsiella oxytoca, Citrobacter freundii complex and Pseudomonas aeruginosa in patients 3 months or older.
Avycaz is also indicated for the treatment of complicated urinary tract infections (cUTI) including pyelonephritis caused by the following susceptible microorganisms: Escherichia coli, Klebsiella pneumoniae, Enterobacter cloacae, Citrobacter freundii complex, Proteus mirabilis, and Pseudomonas aeruginosa in patients 3 months or older.
MBP 184.0 Azedra (iobenguane I 131)
Azedra (iobenguane I 131) is an I 131 labeled iobenguane. Iobenguane is similar in structure to the neurotransmitter norepinephrine (NE) and is subject to the same uptake and accumulation pathways as NE. Iobenguane is taken up by the NE transporter in adrenergic nerve terminals and accumulates in adrenergically innervated tissues, such as the heart, lungs, adrenal medulla, salivary glands, liver and spleen as well as tumors of neural crest origin. Azedra is taken up and accumulates within pheochromocytoma and paraganglioma cells, and radiation resulting from radioactive decay of I 131 causes cell death and tumor necrosis.
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