Glutoxim

NOV-002 in the USA, tradename of Glutoxim in Russia. In clinical trials conducted to date, NOV-002 administered in combination with standard chemotherapeutic regimens has resulted in increased efficacy survival, tumor response) and improved tolerance of standard chemotherapy (e.g. enhanced hematological recovery, immune stimulation).

Dosage	Packing	Price	Add to basket
10 mg (1 ml, 1% solution)	5 ampoules	USD 109.00
20 mg (2 ml, 1% solution)	5 ampoules	USD 124.00
30 mg (1 ml, 3% solution)	5 ampoules	USD 137.00
60 mg (2 ml, 3% solution)	5 ampoules	USD 197.00

Glutoxim: Medications and Prescriptions

Generic name: Glutamyl-Cystinyl-Glycine disodium
Product Brand Name: Glutoxim (in Russia), NOV-002 (in USA)
Product Manufacturer: manufactured in Russia

Glutoxim description

NOV-002, the lead compound acts as a chemopotentiator and a chemoprotectant, in combination with chemotherapy. NOV-002 is approved and marketed in Russia under the trade name Glutoxim®. It has been administered to over 10,000 patients, including clinical studies of 390 patients across many tumor types, demonstrating clinical efficacy and excellent safety data.

NOV-002, the lead compound, acts as a chemopotentiator and a chemoprotectant. NOV-002 was approved in Russia and marketed under the trade name Glutoxim®. NOV-002 has already been administered to over 10,000 patients, including clinical studies of 390 patients across many tumor types, demonstrating clinical efficacy and excellent safety. In one controlled, randomized Russian Phase 2 trial, NOV-002 in combination with cisplatin-based chemotherapy increased the one-year survival of advanced NSCLC patients from 17% to 63% (p < 0.01) and improved tolerance of chemotherapy (p < 0.01) versus the control. In a controlled, randomized U.S. Phase 2 trial, advanced NSCLC patients treated with NOV-002 in combination with paclitaxel and carboplatin demonstrated improved objective tumor response (p < 0.05) and improved tolerance of chemotherapy (p < 0.01) versus the control.

NOV-002 is in Phase 2 development to treat early-stage breast cancer and chemotherapy-resistant ovarian cancer.

Glutoxim, a chemically synthesized biologically active compound, is a hexapeptide with a stabilized disulfide bond (bis-(gamma-L-glutamyl)-L-cisteinyl-bis-glycin disodium salt), total formula – (C20H32O16N6S2).

General information
It has been demonstrated that Glutoxin initiates the cytokine system of normal cells of immunopoiesis and hemopoiesis organs, in particular, it regulates endogenous production of a wide range of interleukins and hematopoietic factors (IL-1b, IL-4, IL-6, IL-8, IL-10,IL-12, TNF, IFN, GM-CSF and erythropoietin) and reproduction of IL-2 effects by inducing IL-2Ra and IL-2Kb receptors.

Reproduction of the effects of a number of cytokines by Glutoxim is of exceptional importance, because diseased characterized by marked immune suppression, such as oncological diseases, are primarily associated with impaired reception of cytokine regulatory effects. The above elements of the drug’s specific activity, including those of its immunomodulationg activity, have been experimentally confirmed in studies of apoptosis regulating mechanisms, in radiation and chemically (cyclophosphane) induced immune deficiency as well as in clinical studies in cancer patients.

Clinical study results make it possible to assume that the basic mechanism of the drug’s general biological activity consists in regulated escalation of the redox state of cells and modification of “critical cysteines” of signal-transmitting systems’ key proteins. The new level of cellular redox contour as well as that of phosphorylation dynamics (cAMP/cGMP ratio) and of nFkB and AP-1 transcription factor activity leads to a chain reaction of genetically determined biochemical mechanisms constituting the functional response of cells to the drug. Thus, in terms of its molecular mechanisms of action the drug can be classified as regulator of redox-sensitive expression of genes, primarily of immunologically relevant ones, which include interleukine-2 (IL-2) alpha chain, tumour necrosis factor alpha (TNFa), alpha and gamma interferons (IFNa,ã), c-fos, Bax and Bcl-2 genes.

Besides, there are experimental and clinical data suggesting that the drug:
- induces differentiation of pre-T lymphocytes (Thy-1 marker) of the bone marrow;
- can activate proliferation and differentiation of normal hemopoietic tissue CD34+ cells and trigger apoptosis-inducing mechanisms in actively proliferating cells in leukemia (as determined by flow cytometry using monoclonal antibodies to Fas-antigen);
The above mechanisms of action account for functional integrity of immunophysiological effects, which include:
- high tropism of the drug to the cells of central immunity organs and of the lymphoid tissue system associated with formation of cytoprotective mechanisms;
- enhancement of erythropoiesis, lymphopoiesis and granulocyte-monocytopoiesis;
- activation of the phagocytosis system, including that in acquired immune deficiency, restoration of neutrophil, monocyte, lymphocyte and platelet counts in peripheral blood;
- predominant activation of T-lymphocyte proliferation and differentiation, also in the situation of radiational and chemical immunosuppression and AIDS, restoration of CD3+, CD4+, CD8+, CD16+/56+ and CD25+ cell counts.
On the whole, Glutoxim can be classified as an immunomodulator possessing multicytokine-activating and hemopoietic activity.

Glutoxim Overview
Glutoxim is approved in Russia for general medicinal use as an immunostimulant in combination with chemotherapy and antimicrobial therapy. Safety and efficacy have been demonstrated in many thousands of cancer, tuberculosis and psoriasis patients. A Phase II lung cancer clinical study was recently completed in USA.

Mechanism of action
Glutoxim effect on major intracellular regulation systems, including the Ras-signal cascade. Glutoxim is the first differentially acting drug which on the one hand acts favourably on normal cells while on the other hand initiating elimination of genetically defective cells (tumour cells or cells affected by viruses) from the body. Genetically defective cells are eliminated due to restoration of their capacity for apoptosis (programmed cell death). In particular, the feect of Glutoxim on genetically intact cells promotes activation of the intracellular proteinkinase cascade, proliferation and restoration of cell susceptibility to humoral factors and mobilizes redox complex enzymes involved in glutathione metabolism (Kozhemyakin et al., 1999). The effect on genetically impaired cells manifests itself in their reaction to humoral factors of apoptosis induction as well as on redox-dependent cell division and apoptosis regulation factors. On molecular level Glutoxim, being a structural analog of oxidized glutathione, activates gluthationereductase, gluthathionetransferase and glutathioneperoxidase, which in their turn activate intracellular reactions of thiolic metabolism and conjugate the processes the synthesis of sulfur- and phosphorous-containing compounds required for normal functioning of intracellular regulatory systems. It is known that cells use an active ATP-dependent system for capturing oxidized glutathione, while the uptake of its reduced from is minimal. Stabilization of oxidized glutathione disulfide bond multiplies its pharmacological effects compared to those of oxidized glutathione.
Experimental and clinical results of the use of Glutoxim have revealed its anti-tumour activity realized through depressing redox potential in transformed cells. It has been demonstrated that redox potential depression can induce apoptosis both due to increased p53 protein half-life and by influencing the cascade of Ras-signal pathway phosphoproteinkinases.

In vitro studies of the effect of Glutoxim on the number of HL60 cells demonstrate that 48 hour incubation in the presence of the drug in the concentration of 100 ug/ml resulted in the death of practically all malignant cells despite defective p53 gene. Addition of Glutoxim to culture medium containing transformed fibroblasts induces apoptosis points to involvement of the Ras-signal cascade in this process. However, while 2 days after of exposure to Glutoxim (C8 cells) in case of cells with enhanced production of Ras-protein and a normally functioning p53 protein death due to apoptosis is almost 100%, in case of defective p53 gene only half the cells died under the same conditions. Thus, apoptosis induction by Glutoxim involves the proteinkinase Ras-signal cascade and follows both p53-dependent and p53-independent pathway. If both the pathways are intact, the effect of Glutoxim is greater than if only one of them functions.

Glutoxim acts on the Ras-signal pathway of an intracellular cascade of phosphorylation of proteins which ultimately trigger cell proliferation. The Ras-signal pathway is characterized by a dual effect of its activation. In normal cells proliferation and differentiation are activated while in malignantly degenerated cells or in cells with impaired GTP-GDP ratio (GTP depletion) capacity for apoptosis increases. This is due to the fact that in the end of the pathway the cascade of Ras-dependent phosphokinase reactions branches out. In normal cells it is the proliferation branch components that are active, while in genetically impaired cells the potentially active branch is that of cell self-destruction, which accounts for the dual effect of the Ras-signal pathway activation by Glutoxim.

Ras-protein activation requires detachment of its C-terminal tripeptide, which takes place due to formation of a high-energy bond between sulfur atoms in the tripeptide cysteine molecule and of phosphorous atoms in the DTP molecule. Acting on this process, Glutoxim contributes to normalization of Ras-protein processing. Only after the cysteine-containing tripeptide is detached does the Ras-protein adequately attach to the cytoplasmic membrane. Besides, the fact that the Ras-signal cascade factors include a number of other GPP-binding proteins containing “critical cysteines” does not exclude its interaction with Glutoxim. The multicomponent effect of Glutoxim on normalizing the Ras-dependent cascade of intracellular reactions proves its preventive role in situations of high oncological risk. Many cytokines act by activating the Ras-signal pathway. Ensuring functional stability of the Ras-signal pathway, Glutoxim contributes to adequate immunocorrection.

Thus, the effect of Glutoxim on key processes of vital functions of cells in a body affected by a tumour promotes both restoration of specific anti-tumour immunity and increased apoptosis of malignant cells. Glutoxim improves the condition of genetically normal cells and initiates elimination of genetically defective ones. It induces a wide range of cellular reactions, including those on genetic level, thus enhancing organism resistance to extreme chemical, physical and biological impacts. The versatility of intracellular regulatory effects of Glutoxim determines its value in treating acute and chronic diseases characterized by hypoxia, cytolysis and impairment of cell proliferation and differentiation ratio.

Preventive use of the drug as a modifier of cellular response to aggressive exogenous and endogenous influences appears equally advisable. Effect of Glutoxim on cell proliferation, differentiation and programmed death via the Ras-signal system. RAS – Ras-protein; P53 – p53-protein; P21 – p21-protein; 1,2,3 – Rho, Rac, Mos guanyl proteins and other proteins influencing the activity of Ras-signal pathway including Raf, MEK, MAPK/ERK, PI 3 phosphokinases.

Dosages
Glutoxim is available as 1% or 3% solution
in 1 ml ampoules containing 10 or 30 mg of the active ingredient, respectively, or
in 2 ml ampoules containing 20 or 60 mg of the active ingredient, respectively.

Storage
at room temp, not above 25 C.

Safety
Experimental single administration of 1000 times the therapeutic dose of the drug as well as chronic (6 months) administration of 100 times the therapeutic dose demonstrated absolute safety of the drug. Glutoxim did not cause negative changes in the major biochemical and physiological systems of the body. The width of Glutoxim therapeutic action is of equal importance. Not a single case of drug withdrawal due to intolerance has been observed during comprehensive clinical studies. Glotoxim has proven to be safe in terms of all criteria used for drug safety evaluation.


Who May Benefit From Glutoxim?
• Cancer patients receiving chemotherapy and/or radiation therapy
• Psoriasis patients
• Tuberculosis patients

What Glutoxim Can Do?
• Improve quality of life
• Reduce chemotherapy toxicity (to bone marrow, blood, liver, kidney and heart)
• Expedite restoration of blood indices and immune system
• Augment effects of chemotherapy
• Prolong life span

What Are Examples of Glutoxim Efficacy in Clinical Studies?
• Lung Cancer - When used in combination with chemotherapy, Glutoxim
increased the one year survival rate from 17% to 63%, increased the tolerability of chemotherapy (as evidenced by 66% increase in the number of cycles) and improved quality of life in lung cancer patients.
• Ovarian Cancer – Glutoxim was able to restore responsiveness to chemotherapy
in women who had failed to respond to standard treatment. In combination with Glutoxim, 80% of the women responded favorably to the same chemotherapy that they previously failed without Glutoxim.
• Psoriasis - Glutoxim is effective in treating severe psoriasis patients. A sevenweek treatment course with Glutoxim (in monotherapy) resulted in a sustained clinical response of over a year in more than 75% of the patients.

What Are the Side Effects of Glutoxim?
Glutoxim is safe! No drug related adverse events have been observed in clinical trials or reported during patient use.

Glutoxim for Psoriasis Patients
In a clinical study with severe psoriasis patients, Glutoxim treated group demonstrated greater than 75% clinical response (measured by no infiltration, no scaling and extended remission period – for 12 months or more). Regression of the skin lesions occurred rapidly with
improvement in just the first 15 days of Glutoxim treatment. Overall treatment period was seven weeks in monotherapy with Glutoxim. No Glutoxim associated adverse effects were observed.

Glutoxim for Tuberculosis Patients
Drug resistant TB patients received either standard TB therapy or Glutoxim plus standard TB therapy. Bacterial discharge cessation (which is a measurement of efficacy) was measured at the end of months 1, 2 and 3. Administration of Glutoxim led to faster disappearance of the tubercle bacteria from sputum (the discharge from respiratory passages), and achieved response in greater
number of patients. Time to Clearance of TB from Sputum in Drug Resistant TB Patients Beneficial effects of Glutoxim were also seen in drug-susceptible TB patients (data not shown). No Glutoxim associated adverse effects were observed.

GLUTOXIM, A DISULFIDE-CONTAINING HEXAPEPTIDE, ENSURES A FAVORABLE SURVIVAL OUTCOME AND BETTER TOLERABlLITY OF CHEMOTHERAPY IN PATIENTS WITH STAGE III-IV NON-SMALL-CELL LUNG CANCER

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

Overview
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 hemotherapy 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%).

Discussion
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).

Glutoxim (NOV-002) in USA:
Novelos Therapeutics, Inc. (OTCBB: NVLT) is a biopharmaceutical company commercializing oxidized glutathione-based compounds for the treatment of cancer and hepatitis. NOV-002, the lead compound currently in Phase 3 development for lung cancer under a Special Protocol Assessment (SPA) and Fast Track, acts together with chemotherapy as a chemopotentiator and a chemoprotectant by regulating redox-sensitive cell signaling pathways. NOV-002 is also in Phase 2 development for early-stage breast cancer and chemotherapy-resistant ovarian cancer. Novelos has a partnership with Mundipharma to develop and commercialize NOV-002 in Europe and Asia (excluding China).

Novelos’ pipeline of drugs is based on oxidized glutathione, a natural metabolite that is part of the glutathione pathway. This pathway is the primary determinant of intracellular redox (oxidation/reduction) potential, and its role in cell detoxification is well studied and understood. More recently, however, it has been recognized as an important physiological regulator of redox-sensitive cell signaling pathways in multiple cell types. Novelos’ lead products are believed to act, in part, via modification of cellular redox status leading to post-translational modification (glutathionylation) of critical regulatory proteins that mediate disease-relevant processes including tumor invasiveness, immune function and blood cell formation.

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Novelos Therapeutics, Inc. (OTCBB: NVLT) is a biopharmaceutical company commercializing oxidized glutathione-based compounds for the treatment of cancer and hepatitis. NOV-002, the lead compound currently in Phase 3 development for lung cancer under a Special Protocol Assessment (SPA) and Fast Track, acts together with chemotherapy as a chemopotentiator and a chemoprotectant by regulating redox-sensitive cell signaling pathways. NOV-002 is also in Phase 2 development for early-stage breast cancer and chemotherapy-resistant ovarian cancer. Novelos has a partnership with Mundipharma to develop and commercialize NOV-002 in Europe and Asia (excluding China). Novelos’ second compound, NOV-205, acts as a hepatoprotective agent with immunomodulating and anti-inflammatory properties. NOV-205 is in Phase 1b development for chronic hepatitis C non-responders. Both compounds have been partnered with Lee’s Pharm in China.


Novelos’ pipeline of drugs is based on oxidized glutathione, a natural metabolite that is part of the glutathione pathway. This pathway is the primary determinant of intracellular redox (oxidation/reduction) potential, and its role in cell detoxification is well studied and understood. More recently, however, it has been recognized as an important physiological regulator of redox-sensitive cell signaling pathways in multiple cell types. Novelos’ lead products are believed to act, in part, via modification of cellular redox status leading to post-translational modification (glutathionylation) of critical regulatory proteins that mediate disease-relevant processes including tumor invasiveness, immune function and blood cell formation.


NOV-002, the lead compound, acts as a chemopotentiator and a chemoprotectant.
NOV-002 was approved in Russia where it is marketed by PharmaBAM under the trade name Glutoxim®. NOV-002 has already been administered to over 10,000 patients, including clinical studies of 390 patients across many tumor types, demonstrating clinical efficacy and excellent safety. In one controlled, randomized Russian Phase 2 trial, NOV-002 in combination with cisplatin-based chemotherapy increased the one-year survival of advanced NSCLC patients from 17% to 63% (p < 0.01) and improved tolerance of chemotherapy (p < 0.01) versus the control. In a controlled, randomized U.S. Phase 2 trial, advanced NSCLC patients treated with NOV-002 in combination with paclitaxel and carboplatin demonstrated improved objective tumor response (p < 0.05) and improved tolerance of chemotherapy (p < 0.01) versus the control. Novelos finalized a SPA with the FDA (May 2006) for a single pivotal Phase 3 trial in advanced NSCLC in combination with first-line chemotherapy, obtained Fast Track designation in August 2006 and commenced the trial in November 2006. Target enrollment of 840+ patients was reached in March 2008 and trial conclusion is expected early 2010. NOV-002 is also in Phase 2 development to treat early-stage breast cancer and chemotherapy-resistant ovarian cancer.


NOV-205, a second compound acts as a hepatoprotective agent with immunomodulating and antiinflammatory properties. Novelos’ IND for NOV-205 as mono-therapy for chronic hepatitis C has been accepted by the FDA, and a U.S. Phase 1b trial in patients who previously failed treatment with pegylated interferon plus ribavirin was concluded based on favorable safety profile. Russian clinical studies in hepatitis B and C patients showed that after relatively short treatment periods (1 to 2 months) with NOV-205, viral load was undetectable in a high proportion of patients and serum biochemical markers of liver damage were significantly decreased.


Novelos' intellectual property is very strong. The intellectual property includes 6 U.S., 2 European and 1 Japanese issued patents. Overall, Novelos has filed more than 30 patent applications worldwide, with coverage including composition of matter, method of use and manufacturing. The breadth of the intellectual property will also allow Novelos to expand its pipeline by claiming and commercializing additional compounds that are based on oxidized glutathione.

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