Medical benefit pharmaceutical policies for providers
See the latest updates to our medical benefit pharmaceutical policies.
MBP 147.0 Lartruvo (olaratumab)
Lartruvo (olaratumab) is a human (recombinant) IgG1 antibody which expressly binds to platelet-derived growth receptor alpha (PDGFR-alpha) to prevent binding of PDGF-AA, PDGF-BB, and PDGF-CC, and block receptor activation and disrupt PDGF receptor signaling. The PDGF-alpha receptor has a role in cell differentiation, growth, and angiogenesis, and has demonstrated antitumor activity in sarcomas.
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 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 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.
New Policy 3/20/18
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.
New Policy 5/15/18
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