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PubMed2006

Noninvasive 1H/13C magnetic resonance spectroscopic imaging of the intratumoral distribution of temozolomide.

Among the primary reasons for failure of anticancer chemotherapy are insufficient drug delivery to the tumor because of inadequate tumor vascularization and/or the antivascular effects of chemotherapy. Thus, determining the spatial intratumoral distribution of anticancer agents by noninvasive methods such as MRI/MRSI is important for monitoring cancer chemotherapy. We therefore studied the distribution of the 13C-labeled anticancer agent temozolomide ([13C]TMZ) in MCF-7 tumor-bearing mice using 1H/13C MRSI. In phantom studies inverse 13C detection with heteronuclear multiple quantum coherence (HMQC) provided a 2.3-fold gain in signal-to-noise ratio (SNR) over direct nuclear overhauser effect (NOE)-enhanced 13C-MRS. This enabled detection of [13C]TMZ in the micromolar range. Three-dimensional (3D) maps of drug distribution with a nominal 2.5-mm isotropic resolution were obtained following intraperitoneal administration of [13C]TMZ, for a total dose of 200 mg/kg. The status of the blood supply of tumors was assessed by gadolinium (Gd)-enhanced dynamic MRI. Nonuniform distributions of the drug and the contrast agent were detected in the tumors. Although carbon-13 MRSI has an inherently low sensitivity for detection, the novel technique described here demonstrates the feasibility of studying the delivery of 13C-labeled drugs and contrast uptake during the course of chemotherapy.

Adenocarcinoma↗
PubMed2006

Whole brain irradiation and temozolomide based chemotherapy in melanoma brain metastases.

INTRODUCTION: Whole brain irradiation (WBRT) remains a recommended treatment for patients with brain metastases from malignant melanoma in terms of symptom palliation, especially when extracranial systemic disease is present. Temozolomide (TMZ) has shown efficacy in the treatment of metastatic melanoma. The objective was to evaluate the potential benefit in survival of two different schedules of total dose and fractionation (20 Gy/5 fractions vs 30 Gy/10 fractions) and further TMZ based chemotherapy. MATERIALS AND METHOD: We have conducted a retrospective study in a group of twenty-one patients (RTOG Recursive Partitioning Analysis class II) of the use of WBRT with 20 Gy/5 fractions (n = 11) and 30 Gy/10 fractions (n = 10). All patients received further TMZ based chemotherapy administered as a single chemotherapeutic agent or in combination with chemo-immunotherapy. RESULTS: Prognostic variables such as: age, Karnofsky performance status, extracranial metastases and number of brain metastases, were analyzed in both groups of treatment without statistically significant differences. The median survival time (MST) for WBRT 20 Gy group was 4 months (CI 95%: range 2- 6 months) and for WBRT 30 Gy group was 4 months (CI 95%: range 0-7 months) without statistically significant differences (Log rank p = 0.74). There was one complete response and two partial responses. CONCLUSIONS: The results suggest that MST was not significantly affected by the total dose/fractionation schedule.

Adult↗
PubMed2007

The Fanconi anemia (FA) pathway confers glioma resistance to DNA alkylating agents.

DNA alkylating agents including temozolomide (TMZ) and 1,3-bis[2-chloroethyl]-1-nitroso-urea (BCNU) are the most common form of chemotherapy in the treatment of gliomas. Despite their frequent use, the therapeutic efficacy of these agents is limited by the development of resistance. Previous studies suggest that the mechanism of this resistance is complex and involves multiple DNA repair pathways. To better define the pathways contributing to the mechanisms underlying glioma resistance, we tested the contribution of the Fanconi anemia (FA) DNA repair pathway. TMZ and BCNU treatment of FA-proficient cell lines led to a dose- and time-dependent increase in FANCD2 mono-ubiquitination and FANCD2 nuclear foci formation, both hallmarks of FA pathway activation. The FA-deficient cells were more sensitive to TMZ/BCNU relative to their corrected, isogenic counterparts. To test whether these observations were pertinent to glioma biology, we screened a panel of glioma cell lines and identified one (HT16) that was deficient in the FA repair pathway. This cell line exhibited increased sensitivity to TMZ and BCNU relative to the FA-proficient glioma cell lines. Moreover, inhibition of FA pathway activation by a small molecule inhibitor (curcumin) or by small interference RNA suppression caused increased sensitivity to TMZ/BCNU in the U87 glioma cell line. The BCNU sensitizing effect of FA inhibition appeared additive to that of methyl-guanine methyl transferase inhibition. The results presented in this paper underscore the complexity of cellular resistance to DNA alkylating agents and implicate the FA repair pathway as a determinant of this resistance.

Antineoplastic Agents, Alkylating↗
PubMed2005

Treatment-related myelodysplastic syndrome after temozolomide for recurrent high-grade glioma.

In patients with recurrent malignant glioma, treatment-related myelodysplastic syndrome (t-MDS) and acute leukemia are rare adverse effects because the median survival after relapse is limited. We report a 44-year-old woman with t-MDS (refractory anemia with excess blasts) following treatment of recurrent anaplastic astrocytoma with temozolomide (TMZ). A cytogenetic study showed del (3)(q11.1). MDS was diagnosed 8.4 months after beginning TMZ. The disease rapidly evolved into acute leukemia within 1 month after the onset of MDS, and the patient died 1 month later during induction chemotherapy. The prognosis of t-MDS is generally poor. Considering the increasing use of TMZ, which is regarded as a drug with moderate toxicity, careful follow-up with routine blood testing is vital.

Acute Disease↗
PubMed2006

Phase II trial of temozolomide in children with recurrent high-grade glioma.

PURPOSE: The objective of the study was to evaluate the efficacy and toxicity of Temozolomide (TMZ) administered for 5 consecutive days in three daily dosing in children with recurrent or refractory high-grade glioma. PATIENTS AND METHODS: Twenty-four patients with a median age of 10.5 years were enrolled onto this open-label, multicenter, phase II study. The patients were previously treated with surgical resection (17 of 24), radiotherapy (19 of 24) and chemotherapy (18 of 24). Therapy was administered orally three times a day for 5 consecutive days at the dose of 200 mg/m(2)/dx5 for chemotherapy naive patients. In patients heavily pretreated with chemotherapy the starting dose was of 150 mg/m(2)/dx5. RESULTS: A total of 95 cycles were administered. The median progression free-survival (PFS) was 3 months for the entire group while disease stabilization was obtained in 7 patients (29.1%), all with supratentorial tumors. No CR or PR was observed. TMZ treatment showed a limited toxicity. Thrombocytopenia was the most common hematological adverse effect. Our data suggest a marginal activity of TMZ in children with recurrent high-grade glioma.

Adolescent↗
PubMed2006

Phase II trial of temozolomide plus marimastat for recurrent anaplastic gliomas: a relationship among efficacy, joint toxicity and anticonvulsant status.

PURPOSE: Since anaplastic gliomas (AG) depend on matrix metalloproteinases for tumor cell invasion and angiogenesis, we undertook this phase II study to evaluate the matrix metalloproteinase inhibitor marimastat (MT), combined with the alkylator temozolomide (TMZ) in patients with recurrent AG, looking for improved outcomes. PATIENTS AND METHODS: Patients were treated every 28 days with TMZ at 150-200 mg/m2 once daily on days 1-5 and MT at 25 mg twice daily on days 8-28. Results were compared to our database of anaplastic glioma patients treated at recurrence. A subanalysis of the relationship between MT-induced joint-related toxicity and anticonvulsant status was carried out. RESULTS: Forty-nine patients were enrolled; all were assessable for toxicity, and 46 were included in the efficacy analysis. Joint and muscle complaints occurred in 32 patients (65%); 1 patient was removed from the study due to toxicity. The best protocol response was a complete response in 1 patient and a partial response in 2 patients (3/46=7%, 95% confidence interval (CI)=1, 18). Median time to progression was 24 weeks (95% CI=16, 56), and the progression-free survival (PFS) rate was 48% at 6 months (95% CI=35%, 65%), which surpassed the protocol objective of 40%. Sub-analysis showed a positive impact of joint-related toxicity due to MT on PFS whether or not patients were taking CYP450 enzyme-inducing anticonvulsants. CONCLUSIONS: Even though this regimen is more efficacious than our comparator of historical controls in recurrent AG, the regimen was roughly equivalent to single-agent TMZ and was associated with additional toxicity. The sub-analysis suggests pharmacokinetic and drug-drug interactions which may positively impact responses to MT.

Anticonvulsants↗
PubMed2006

Predictive and prognostic markers in human glioblastomas.

Glioblastomas (GBMs) are among the most aggressive of all known human tumors. The median survival times remain in the 12- to 15-month range despite aggressive surgery, radiation, and chemotherapy. Through molecular and genetic profiling efforts, underlying mechanisms of resistance to these therapies are becoming better understood. The present standard of care has been shaped by the recently reported phase III study by the European Organisation for Research and Treatment of Cancer and the National Cancer Institute of Canada, which found that the addition of temozolomide (TMZ) to radiation therapy significantly improved outcome compared with radiation alone. However, careful examination of these data reveals that not all GBM patients benefited from the addition of TMZ to radiation therapy. A companion correlative study found that GBM patients with tumors with MGMT promoter methylation appeared to derive the greatest benefit from the addition of TMZ to radiation therapy. Although this finding is provocative, it should be kept in mind that this study was performed retrospectively and that prospective validation is required before MGMT methylation can be used for clinical stratification purposes. However, this study does show promise for the tailoring of future treatments according to the molecular and genetic profiles of an individual's tumor rather than using the "one-glove-fits-all" approach that is currently being followed. As more effective "smart drugs" are developed, molecular and genetic profiling will assume even greater importance in this regard.

Biomarkers, Tumor↗
PubMed2005

Optimal role of temozolomide in the treatment of malignant gliomas.

Temozolomide (TMZ) is an alkylating agent that was approved for anaplastic astrocytoma and glioblastoma. Its role in the treatment of recurrent disease has been confirmed, and more importantly, alternative treatment schedules and combination regimens have been developed. A recent phase III trial has demonstrated a survival advantage for concomitant TMZ administration with radiotherapy in patients with newly diagnosed glioblastoma. Molecular studies suggest a strong predictive role of the DNA repair enzyme O6-methyl-guanine-DNA-methyl-transferase (MGMT) and outcome of TMZ-based chemotherapy. This review summarizes the current knowledge, highlights approved and nonapproved indications, and describes molecular studies that may allow us to identify the patients most likely to benefit from this treatment.

Antineoplastic Agents, Alkylating↗
PubMed1991

Assessment with potential mapping of the cardiac protective effect of a drug. Example of trimetazidine.

SATAPEC is a computerized system built in the Laboratory for recording over 256 multiplexed channels and for automatic processing of cardiac electrical potentials. The results are printed out in the form of maps (either in black and white or in color) showing potential distributions, depolarization, repolarization, duration of activation, or various other analog-digital data. The cardioprotective ability of a drug may be assessed with SATAPEC. As an example, the effect of trimetazidine (TMZ) is examined using 2 groups of 12 rabbits (one group serving as a control and the second group pretreated with TMZ). An elastomer mesh with 240 regularly spaced chlorided silver wire electrode is placed around the ventricles following thoracotomy. A ligature is made starting from the anterior interventricular artery (AIV). Recordings are taken from the 240 unipolar epicardial electrograms (reference potential taken at Wilson terminal) 1 min before ligation and then every min for 8 min following ligation. Once the electrograms are plotted and any aberrant tracings eliminated, ST variation is calculated automatically. Files containing ST variations at different instants are stored in the computer memory and the mean sigma ST/240 curves of the two groups of rabbits are plotted versus time. Mean electric potential maps, obtained by aligning all of the individual maps, are then printed. With these maps the location and extent of the epicardial injured area can be visualized. Pretreatment with TMZ (2.5 mg/kg) has shown a beneficial effect on ischemia injury.

Animals↗
PubMed2004

Phase II study of temozolomide and thalidomide with radiation therapy for newly diagnosed glioblastoma multiforme.

PURPOSE: The chemotherapeutic agent temozolomide (TMZ) and the antiangiogenic agent thalidomide have both demonstrated antitumor activity in patients with recurrent malignant glioma. The objectives of this study were to determine if the combined strategy of these oral agents with radiation therapy (RT) is associated with an improved median survival of patients with newly diagnosed glioblastoma multiforme and to evaluate toxicity. METHODS AND MATERIALS: Sixty-seven patients were enrolled in this trial. Radiotherapy parameters were a total dose of 60 Gy delivered in 2 Gy fractions over 6 weeks. Temozolomide was administered starting the first day of RT at 150 mg/m(2) daily for 5 days every 4 weeks for the first cycle and escalated to a maximum dose of 200 mg/m(2). Thalidomide was started on Day 7 of RT at 200 mg and escalated by 100-200 mg every 1-2 weeks depending on patient tolerance, to a maximum of 1,200 mg daily. RESULTS: Sixty-one patients have progressed, with a median time to progression of 22 weeks. Fifty-six patients have died, and the median survival was 73 weeks. CONCLUSIONS: This strategy of combination TMZ, thalid and RT was relatively well tolerated with favorable survival outcome for patients with GM when compared to patients not treated with adjuvant chemotherapy and similar to those who have received nitrosourea adjuvant chemotherapy. It is unclear the added advantage thalid has in combination with TMZ for this patient population.

Adult↗
PubMed1998

Role of cDNA-expressed human cytochromes P450 in the metabolism of diazepam.

The metabolic conversion of diazepam (DZ) to temazepam (TMZ, a C3-hydroxylation product of DZ) and N-desmethyldiazepam (NDZ, an N1-demethylation product of DZ) was studied using cDNA-expressed human cytochrome P450 (CYP) isozymes 1A2, 2B6, 2C8, 2C9, 2C9R144C, 2E1, 3A4, and 3A5 and human liver microsomes from five organ donors. Of the CYPs examined, 3A5, 3A4, and 2B6 exhibited the highest enzymatic activities with turnovers ranging from 7.5 to 12.5 nmol of product formed/min/nmol for the total metabolism of DZ, while 2C8, 2C9, and 2C9R144C showed lesser and moderate activities. 1A2 and 2E1 produced insignificant amounts of metabolites of DZ. The regioselectivity of CYPs was determined, and 2B6 was found to catalyze exclusively and 2C8, 2C9, and 2C9R144C preferentially the N1-demethylation of DZ to form NDZ. 3A4 and 3A5 catalyzed primarily the C3-hydroxylation of DZ, which was more extensive than the N1-demethylation. The ratios of TMZ to NDZ formed in the metabolism of DZ by 3A4 and 3A5 were approximately 4:1. Enzyme kinetic studies indicated that 2B6- and 2C9-catalyzed DZ metabolism followed Michaelis-Menten kinetics, whereas 3A4 and 3A5 displayed atypical and non-linear curves in Lineweaver-Burk plots. Human liver microsomes converted DZ to both TMZ and NDZ at a ratio of 2:1. Our results suggest that hepatic CYP3A, 2C, and 2B6 enzymes have an important role in the metabolism of DZ by human liver.

Cytochrome P-450 Enzyme System↗
PubMed2002

Effects of trimetazidine on tissue damage in kidney after hindlimb ischemia-reperfusion.

The objective of this study was to investigate the effects of trimetazidine (TMZ) on tissue damage in kidney after hindlimb ischemia-reperfusion (I/R), by assessing blood biochemical assay and histopathological analysis. Adult male Wistar rats were divided into two groups. TMZ 10 mg kg(-1)day(-1) was administrated twice a day for 10 days to the treatment group (group T, n=10). Sham group was given only 5% gum arabic (group S, n=10). On 11th day of treatment, 8h I/R period was performed on right hindlimb of the rats. At the end of reperfusion period, a 5 ml blood withdrawn from ascending aorta for biochemical assays and their right kidneys were harvested for histopathological examination. Superoxide dismutase, Na(+)-K(+) ATPase, and reduced glutathione levels were significantly increased in group T (P<0.001). On the other hand, myeloperoxidase and malondialdehyde levels were significantly less in group T than group S (P<0.001). Kidneys from the sham-operated group displayed intense leukocytic infiltration in histopathological examination. These overall results strongly suggested that TMZ contributes renal protection from hindlimb I/R injury by decreasing systemic oxidative stress.

Animals↗
PubMed2004

[Survival analysis following the addition of temozolomide to surgery and radiotherapy in patients with glioblastoma multiforme].

OBJECTIVES: To analyze the effect of different therapies -surgery, radiotherapy, and chemotherapy (temozolomide)- on the survival of various groups of patients with glioblastoma multiforme (GBM). METHOD: The overall survival of a total of 85 patients with histopathological diagnosis of GBM was analyzed (descriptive statistics, Kaplan-Meier). Patients were divided into 4 treatment groups: group 1 (n=12), untreated patients (" no treatment" option was chosen by the family); group 2 (n=22), patients undergoing surgery only (retrospective series from the 1980s); group 3 (n=24), patients undergoing surgery + standard radiotherapy (control group, partially effective treatment); group 4 (n=27), patients undergoing surgery + radiotherapy + chemotherapy (temozolomide [TMZ]) (current study group). RESULTS: Mean age (one-way ANOVA) showed no significant difference between the groups. Mean/median survival (weeks) was as follows: group 1, 18/16; group 2, 23/14; group 3, 48/42; group 4, 70/64. The Kaplan-Meier analysis yielded the following 50% survival cutoffs (weeks): group 1, 16.00; group 2, 14.29; group 3, 42.00; group 4, 64.43. This demonstrated a significant difference when radiotherapy (group 3) was added to surgery (group 2) or no treatment (group 1), and a significant difference (p < 0.001) in survival when TMZ (group 4) was added to the so far considered as being the standard treatment (group 3: surgery + radiotherapy). CONCLUSIONS: Surgery alone does not result in a higher survival rate for GBM patients. However, surgery allows to establish a histopathological diagnosis, to improve signs and symptoms which are attributable to intracranial hypertension or tumour topography, and to reduce the number of target cells for adjunctive therapies. Radiotherapy improves survival and TMZ chemotherapy that is given after radiotherapy adds further survival benefit for patients.

Antineoplastic Agents, Alkylating↗
PubMed1998

Delivery of cytotoxic drugs from carrier cells to tumour cells by apoptosis.

A new drug delivery approach, apoptotic-induced drug delivery (AIDD), is presented that is based on apoptosis as a mechanism to trigger delivery of drugs from carrier cells. It was investigated whether apoptotic drug-loaded carrier cells could deliver drugs to tumour cells by various mechanisms, including drug release through a more permeable apoptotic cell membrane, and by phagocytosis of drug-loaded apoptotic cells by tumour cells. The feasibility of this novel concept was evaluated in an in vitro carrier cell model that consisted of S49 mouse lymphoma cells that apoptose upon exposure to dexamethasone (DX). Membrane permeability was evaluated by measurement of release of a fluorescent dye (calcein-AM, C-AM) from C-AM-loaded S49 cells. Phagocytotsis of fluorescent PKH-26-labeled S49 cells was determined in co-culture studies with rat glioma (RG-2) cells using fluorescence microscopy and flow cytometry. Cytotoxicity of RG-2 cells due to temozolomide (TMZ)-loaded S49 cells was evaluated by a colony formation assay following co-culture of these cells for up to 8h. Calcein release from S49 cells was enhanced by approximately 30% at 48 h following treatment with DX compared to control S49 cells. Based on both flow cytometric and microscopic analyses, RG2 phagocytized apoptotic S49 cells to a four- to sevenfold greater extent than control S49 cells at co-incubation times from 4-48 h. The TMZ-loaded apoptotic S49 cells caused the largest degree of toxicity, about 50% cell kill, whereas TMZ-loaded control S49 caused 30% cell kill. The preliminary data suggest that AIDD should be further explored.

Journal Article↗
PubMed2004

Phase II trial of cisplatin plus temozolomide, in recurrent and progressive malignant glioma patients.

We report a phase II trial of cisplatinum and temozolomide (TMZ) combination in recurrent malignant glioma patients. The DNA repair protein O(6)-alkylguanine-DNA alkyltransferase (AGAT) is important in glioblastoma resistance to alkylating antitumor agents. In vitro, cisplatin (CDDP) decreases MGMT activity in a time- and dose-dependent manner. Thirty-three recurrent malignant glioma patients (20 GBM-13 AA) were treated at recurrence or progression with a CDDP and TMZ association. On days 1 and 2, iv CDDP (40 mg/sqm) was administered. TMZ (at the dose of 200 mg/sqm) was administered as a single oral daily-dose on days 2-6 (starting 24 h after the first CDDP dose), the cycle was repeated every 4 weeks. All patients had been previously treated with surgery followed by radiotherapy and CDDP + BCNU chemotherapy. The primary endpoint of the study was progression free survival at 6 months (PFS-6). Secondary endpoints included radiological response and toxicities. Thirty-three patients received a total of 113 courses (median 3 range 1-11). Complete responses were not observed, partial responses were 18.8% with an additional 39.9% of stable disease. For the whole group of patients the PFS at 6 and 12 months was 52% and 15% with a median TTP of 33 weeks. PFS-6 for GBM and Anaplastic astrocytoma (AA) were 35% and 69%, respectively. PFS-12 for GBM and AA were 13.8% and 17.3%, respectively. Median TTP was 21.3 and 39.5 weeks, respectively. The principal toxic effects of the regimen were: neutropenia (5 WHO grade IV), thrombocytopenia (4 WHO grade IV), nausea and vomiting.

Adult↗
PubMed2002

The treatment of brain metastases from malignant melanoma.

Metastasis to the CNS develops in nearly half of patients with advanced melanoma; in 15% to 20% of these patients, the CNS is the first site of relapse. While systemic therapy for metastatic melanoma produces objective responses in 15% to 50% of patients, the available drugs do not penetrate well into the CNS, and these patients rarely benefit from systemic therapy. Although brain metastasis may be treated with surgery and/or stereotactic radiosurgery (SRS) when disease is limited to approximately one to three lesions, treatment for patients with large or multiple metastases is limited to whole brain irradiation (WBRT). While formal response and survival analyses of the impact of WBRT in melanoma have not been reported, the estimated median survival time for unselected patients with CNS metastases is only 2 to 4 months, with 1-year survival rates of less than 13%. In a selected population of patients with limited CNS involvement, surgical resection alone or in combination with WBRT appears to prolong median survival. More recently, SRS has been shown to be an effective local treatment for selected patients with brain metastases. In several retrospective reports of patients with melanoma CNS metastases, treatment with surgical resection alone or in combination with WBRT has been demonstrated to prolong median survival. More recently, SRS has been shown to be an effective local treatment for selected patients with brain metastases. In several retrospective reports, patients with CNS metastases from melanoma treated with a combination of WBRT plus SRS or SRS alone had median survivals and rates of control in the CNS superior to published reports for traditional WBRT. Most of these patients died from progressive extracranial disease with locally controlled CNS disease. Investigation of the contribution of newer systemic agents to the control of melanoma metastatic to the CNS has been based on the identification of drugs that have antitumor activity and the ability to cross the blood-brain barrier. Fotemustine is a nitrosourea that produced similar activity in CNS metastasis as in systemic disease, with a response rate of about 25%. Temozolomide (TMZ) is an oral alkylating agent that acts via the same mechanism as dacarbazine (DTIC), the most active single agent in melanoma. TMZ, which is highly active in brain tumors, has also been associated with activity in systemic and CNS metastases in melanoma patients, also in the 25% range. Efforts are underway to assess the additive benefit of TMZ and other drugs to WBRT or focused radiotherapy in this disease.

Antineoplastic Agents↗
PubMed1980

Long-term vasodilator therapy with trimazosin in chronic cardiac failure.

Patients with cardiac failure have a generalized sympathetic vasoconstriction that may impair cardiac function and exercise tolerance. The ability of long-term alpha-receptor blockade and vasodilation with trimazosin (TMZ) to improve exercise capacity was studied in patients with chronic, stable heart failure of varying severity (functional exercise classes B to D). Exercise performance was monitored by respiratory gas exchange and air flow before and after patients were randomized to placebo (13 patients) or TMZ were then followed on treatment for up to 52 weeks. Significant (P less than 0.05) and sustained increases in exercise capacity, oxygen uptake, and oxygen pulse were observed with TMZ treatment in each Class B or C patient and in six of nine Class D patients, and were not observed during treatment with placebo.

Adrenergic alpha-Antagonists↗
PubMed2003

Somatosensory evoked potential and histopathological investigations in ischaemia-induced brain damage: effects of trimetazidine in rats.

We studied the protective effects of trimetazidine (TMZ) on brain damage by means of somatosensory evoked potentials (SEP) in rats. The TMZ group did not show any statistically significant difference from the control group with respect to SEPs. However, the percentage of cells with ischaemic cell damage in hippocampal regions was significantly smaller in the TMZ group than the control group. Trimetazidine reduced the number of damaged cells in the cerebral tissue during the ischaemia-reperfusion damage. It was suggested that higher doses of trimetazidine may further reduce the number of cells with ischaemic damage.

Animals↗