Medical benefit pharmaceutical policies for providers
See the latest updates to our medical benefit pharmaceutical policies.
MBP 125.0 Lemtrada (alemtuzumab)
Lemtrada (alemtuzumab) is a CD52-directed cytolytic monoclonal antibody indicated for the treatment of patients with relapsing forms of multiple sclerosis (MS). Because of its safety profile, the use of Lemtrada should be generally reserved for patients who have had an inadequate response to two or more drugs indicated for the treatment of MS.
MBP 254.0 Leqvio (inclisiran)
Inclisiran is a small interfering ribonucleic acid, conjugated on the sense strand with triantennary N-Acetylgalactosamine to facilitate uptake by hepatocytes. In hepatocytes, inclisiran utilizes the RNA interference mechanism and directs catalytic breakdown of mRNA for PCSK9. This increases low-density lipoprotein-cholesterol (LDL-C) receptor recycling and expression on the hepatocyte cell surface, which increases LDL-C uptake and lowers LDL-C levels in the circulation.
MBP 288.0 Leqembi (lecanemab-irmb)
Leqembi (lecanemab-irmb) is a humanized monoclonal antibody directed against aggregated soluble and insoluble forms of amyloid beta. Lecanemab reduces amyloid beta plaques, the accumulation of which is a defining pathophysiological feature of Alzheimer disease.
New Policy 5/16/23
MBP 186.0 Libtayo (cemiplimab-rwlc)
Libtayo (cemiplimab-rwlc) is a recombinant human IgG4 monoclonal antibody that inhibits programmed death-1 (PD-1) activity by binding to PD-1 and blocking the interactions with the ligands PD-L1 and PD-L2, releasing PD-1 pathway-mediated inhibition of immune response, including anti-tumor response. PD-1 ligand upregulation may occur in some tumors and signaling through this pathway can contribute to inhibition of active T-cell immune surveillance of tumors. Blocking PD-1 activity has resulted in decreased tumor growth.
MBP 47.0 Lucentis (ranibizumab), Byooviz (ranibizumab-nuna), and Cimerli (ranibizumab-eqrn)
Ranibizumab is a recombinant humanized monoclonal antibody fragment which binds to and inhibits human vascular endothelial growth factor A (VEGF-A). Ranibizumab inhibits VEGF from binding to its receptors and thereby suppressing neovascularization and slowing vision loss.
MBP 83.0 Lumizyme (alglucosidase alfa)
Lumizyme (alglucosidase alfa) is a lysosomal glycogen-specific enzyme indicated for patients with Pompe disease [acid alpha-glucosidase (GAA) deficiency]. Lumizyme (alglucosidase alfa) provides an exogenous source of GAA allowing conversion of glycogen to energy in heart and muscle cells.
MBP 189.0 Lumoxiti (moxetumomab pasudotox-tdfk)
Lumoxiti (moxetumomab pasudotox-tdfk) is a CD22-directed cytotoxin composed of a recombinant murine immunoglobulin genetically fused to truncated Pseudomonas exotoxin (PE38). Moxetumomab pasudotox-tdfk binds CD22 on the cell surface of B-cells and is internalized. Moxetumomab pasudotox-tdfk internalization results in ADP-ribosylation of elongation factor 2, inhibition of protein synthesis, and apoptotic cell death.
MBP 280.0 Lunsumio (mosunetuzumab-axgb)
Lunsumio (mosunetuzumab-axgb) is a T-cell engaging bispecific humanized monoclonal antibody that binds to the CD3 receptor expressed on the surface of T-cells and CD20 expressed on the surface of lymphoma cells and some healthy B-lineage cells. Mosunetuzumab activates T-cells, releasing proinflammatory cytokines, and inducing B-cell lysis.
New Policy 5/16/23
MBP 170.0 Lutathera (lutetium Lu 177 dotatate)
Lutathera (lutetium Lu 177 dotatate) is a beta- and gamma-emitting radionuclide which binds to somatostatin receptors with highest affinity to subtype 2 receptors (SSRT2). Upon binding to somatostatin receptor expressing cells, including malignant somatostatin receptor-positive tumors, the compound is internalized. The beta emission form Lu 177 induces cellular damage by formation of free radicals in somatostatin receptor-positive cells and in neighboring cells.
MBP 174.0 Luxturna (voretigene-neparvovec-rzyl)
Luxturna (voretigene-neparvovec-rzyl) is an adeno-associated virus vector-based gene therapy that delivers a normal copy of the gene encoding human retinal pigment epithelial 65 kDa protein (RPE65) to retinal cells thus augmenting reduced or absent levels of biologically active RPE65. The RPE65 gene mutations lead to reduced or absent levels of RPE65 isomerohydrolase activity, blocking the visual cycle and ultimately impairing vision.
Learn more about Geisinger Health Plan.
Log in to NaviNet to access and view prior authorization information.
Clinical guidelines offer providers consistent and appropriate guidance for diagnosis and treatment of specific conditions or diseases.
Terms and conditions
View GHP’s terms and conditions.
Questions? Contact us
If you have questions or need more information, contact Geisinger Health Plan.