Latest research on G-CSF

Filgrastim is a recombinant, non-pegylated human granulocyte colony stimulating factor (G-CSF) analogue manufactured by recombinant DNA technology using a strain of E. coli. It is marketed as the brand name Neupogen by Amgen. Chemically, it consists of 175 amino acid residues. The protein has an amino acid sequence that is identical to the natural sequence predicted from human DNA sequence analysis, except for the addition of an N-terminal methionine necessary for expression in E coli. Tbo-filgrastim, which is marketed by Sicor Biotech and FDA approved on August 29, 2012, contains the same active ingredient as Neupogen and is biologically similar, but it is formulated to be short-acting. On March 6, 2015, the FDA approved the biosimilar Zarxio (filgrastim-sndz) and is indicated for use in the same conditions as Neupogen. Zarxio is marketed by Sandoz.

G-CSF indications

In this case, we report co-administration of intrathecal cultured mesenchymal stem cells, and subcutaneous G-CSF (Derakhshanrad et al., 2013) in a patient with acute penetrative SCI and in the follow up, the neurological and functional outcomes (Steeves et al., 2007) as well as the observed adverse effects are reported. [source, 2015]
Despite their recognized efficacy, the major drawback of using the traditional pyrethroid spraying is its limited effectiveness in certain regions, such as the Gran Chaco area [5]. [source, 2015]
Although the traditional Chinese medicine Angelicae sinensis is commonly used to promote erythropoiesis for the treatment of anemia, and FA has previously been demonstrated to increase the levels of EPO and G-CSF (8,9), the results of the present study suggest that the neuroprotective effect of FA is not associated with G-CSF. [source, 2015]
Recombinant granulocyte-colony stimulating factors (G-CSF), such as filgrastim (Neupogen), may be effective in treating leukopenia/neutropenia cuased by chemotherapy with Valganciclovir or ganciclovir. [source, 2015]
The effect of Tbo-filgrastim on ECG parameters in healthy subjects was evaluated in two previous Phase I studies that demonstrated no significant ECG changes as a result of treatment (data on file, Teva Pharmaceuticals). [source, 2015]
However, these studies were not powered to allow a conclusive evaluation of the effects of Tbo-filgrastim on cardiac repolarization. [source, 2015]
The primary objective was to assess the effect of a single 5 μg/kg intravenous infusion of Tbo-filgrastim on ventricular repolarization and other ECG parameters in healthy subjects. [source, 2015]
Secondary cardiac end points included the placebo-corrected time-matched changes from baseline for HR, PR interval, and QRS interval, as well as changes in ECG morphologic patterns and concentration-effect analysis of the relationship between QTcI change from baseline and serum concentrations of Tbo-filgrastim. [source, 2015]
For the comparison of Tbo-filgrastim versus placebo, a real prolongation effect of 3 milliseconds maximum was assumed, as this is a commonly used estimate of difference for drugs that have a negative cardiac risk in preclinical studies and is required to demonstrate a significantly shorter effect than 10 milliseconds, as supported by the ICH E14 guidance. [source, 2015]
Pharmacokinetic effects on cardiac end points were evaluated in all subjects who received Tbo-filgrastim and had digital ECG data collected before study-drug administration and at one or more time points after study-drug administration, as well as a time-matched serum concentration. [source, 2015]