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Glutoxim, a disulfide-containing hexapeptide, ensures a favorable survival outcome and better tolerability of chemotherapy in patients with stage III-IV non-small-cell lung cancer.


Kozhemyakin LA., Smirnov A.I., Orlov S.V. Pulmonology Research Institute of Saint-Petersburg State Pavlov Medical University, St-Petersburg, Russia, Novelos Therapeutics, Inc., USA.



Glutoxim, a hexapeptide with a stabilized disulfide bond, has been shown to possess multicytokine-activating and hematopoietic properties and has been recently approved for medicinal use in the Russian Federation. The medicine was also demonstrated to be capable of potentiating conventional chemotherapy presumably due to influencing MDR, p53, and p21 gene systems. Efficacy and safety of Gluloxim were evaluated in NSCLC Stage III-IV patients enrolled into 2 prospective randomized open label studies looking at tolerability of chemotherapy and tumor response, hematopoietic recovery, and survival (respectively, 30 and 42 patients were enrolled, 68 and 37 found available). Results of the randomized studies along with retrospective data on more than 140 other NSCLC patients having received Gluloxirn substantiate the idea of using the medicine in NSCLC as a supportive add on treatment in prevent chemotherapy intolerability and resistance, as well as to ensure beneficial survival outcome.

Study Population and Dosing Regimens.
By now the clinical data on NSCLC patients treated with Glutoxim have been collected for more than 200 individuals. About 60 of them received Glutoxim as an add-on treatment in the framework of the 2 above mentioned prospective randomized studies, while findings on more than 140 other patients have been analyzed retrospectively as observational cases. The patients randomized into the control groups of the prospective randomized studies were treated with chemotherapy alone (cisplatin - etopozid regimens). The subjects randomized into the active treatment arms received identical chemotherapy regimens combined with Glutoxim applied as intravenous or intramuscular injections (30-90 mg. daily). The other 140 patients received treatment with Gluloxim (30-120 mg) combined with various chemotherapy regimens and sometimes with radiotherapy applied before or after the chemotherapy. These observational data have been analyzed against a retrospectively compiled control group of 118 patients who received chemo- or chemo- plus radiotherapy without Glutoxim.

Main Results.

The analysis performed for the 2 prospective randomized studies and for retrospective observations have revealed certain trends in safety and efficacy profiles of Glutoxim, which proved to be common for all 3 patient cohorts. First, there have been no study related adverse events, laboratory abnormalities or incompatibility with any other class of medicines used in the treatment of cancer patients. Second, patients treated with Clutoxim experienced less prominent hemodepression in response to the chemotherapy and faster hematopoietic recovery than in the control group. This mitigation by Glutoxim of the sine- ejects associated with chemotherapy prevents treatment-related complications and allows patients to receive additional courses of chemotherapy more frequently. Thus, patients treated with Glutoxim were able to tolerate more chemotherapy courses and higher doses of the anticancer drugs. Third, a measurable tumor response was detected for a greater number for sequential chemotherapy courses, with the overall response being more prominent for the Glutoxim groups than in the control ones. Finally, a survival analysis for the first prospective randomized study showed that by the end of 1-year follow-up just 5 patients out of 30 available control subjects (16.7%) had survived, while in the Glutoxim group there had been 24 patients out of the 38 available, who had survived for 1 year (63.2%).


The above results will be discussed in the context of other recently collected clinical and experimental data on interaction of disulfide-containing peptides with intracellular regulatory mechanisms of normal and cancer ceils (RAS signaling cascade, MDR-. p53-, and p21-gene systems' and redox-dependent transcription factors).


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