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EC number: 245-826-4 | CAS number: 23694-14-6
- Life Cycle description
- Uses advised against
- Endpoint summary
- Appearance / physical state / colour
- Melting point / freezing point
- Boiling point
- Density
- Particle size distribution (Granulometry)
- Vapour pressure
- Partition coefficient
- Water solubility
- Solubility in organic solvents / fat solubility
- Surface tension
- Flash point
- Auto flammability
- Flammability
- Explosiveness
- Oxidising properties
- Oxidation reduction potential
- Stability in organic solvents and identity of relevant degradation products
- Storage stability and reactivity towards container material
- Stability: thermal, sunlight, metals
- pH
- Dissociation constant
- Viscosity
- Additional physico-chemical information
- Additional physico-chemical properties of nanomaterials
- Nanomaterial agglomeration / aggregation
- Nanomaterial crystalline phase
- Nanomaterial crystallite and grain size
- Nanomaterial aspect ratio / shape
- Nanomaterial specific surface area
- Nanomaterial Zeta potential
- Nanomaterial surface chemistry
- Nanomaterial dustiness
- Nanomaterial porosity
- Nanomaterial pour density
- Nanomaterial photocatalytic activity
- Nanomaterial radical formation potential
- Nanomaterial catalytic activity
- Endpoint summary
- Stability
- Biodegradation
- Bioaccumulation
- Transport and distribution
- Environmental data
- Additional information on environmental fate and behaviour
- Ecotoxicological Summary
- Aquatic toxicity
- Endpoint summary
- Short-term toxicity to fish
- Long-term toxicity to fish
- Short-term toxicity to aquatic invertebrates
- Long-term toxicity to aquatic invertebrates
- Toxicity to aquatic algae and cyanobacteria
- Toxicity to aquatic plants other than algae
- Toxicity to microorganisms
- Endocrine disrupter testing in aquatic vertebrates – in vivo
- Toxicity to other aquatic organisms
- Sediment toxicity
- Terrestrial toxicity
- Biological effects monitoring
- Biotransformation and kinetics
- Additional ecotoxological information
- Toxicological Summary
- Toxicokinetics, metabolism and distribution
- Acute Toxicity
- Irritation / corrosion
- Sensitisation
- Repeated dose toxicity
- Genetic toxicity
- Carcinogenicity
- Toxicity to reproduction
- Specific investigations
- Exposure related observations in humans
- Toxic effects on livestock and pets
- Additional toxicological data
Carcinogenicity
Administrative data
Description of key information
Levosulpiride was not found to be carcinogen in both rats and mice.
Key value for chemical safety assessment
Carcinogenicity: via oral route
Link to relevant study records
- Endpoint:
- carcinogenicity: oral
- Type of information:
- experimental study
- Adequacy of study:
- key study
- Reliability:
- 4 (not assignable)
- Rationale for reliability incl. deficiencies:
- secondary literature
- Guideline:
- other: not specified
- GLP compliance:
- not specified
- Conclusions:
- Levosulpiride was not found to be carcinogen in both rats and mice.
- Executive summary:
The oncogenic/carcinogenic toxicity of levosulpiride was tested in 600 Wistar rats and NMRI mice by long-term oral administration. 200 further rats and 200 further mice served as controls. Levosulpiride was given over 104 weeks in rats and 100 weeks in mice in daily dosage of 12.5, 25.0 and 50.0 mg/kg/day in the food. The control rats and mice remained untreated. The final mortality was significantly higher, in respect to controls, in rats and mice treated with levosulpiride at the dose of 50.0 mg/kg/day and it was similar or identic to controls in the groups treated with levosulpiride at doses of 12.5 and 25.0 mg/kg/day. The researches in rats showed that the lowest and medium tested dosage of levosulpiride (12.5 and 25.0 mg/kg/day in the food) were in the range of the estimated good tolerated doses and did not influence the behaviour, the external appearance, the faeces, the mortality, the food and drinking water consumption, the haematological and urinary profiles, the body weight development, the weight of examinated organs, sight, hearing, dentition and the number of palpable masses. The highest dose of levosulpiride (50.0 mg/kg/day in the food) did not modify the behaviour, the external appearance, faeces, the drinking water consumption, the haematological and urinary profiles, sight, hearing, dentition or the number of palpable masses, but it induced a significant decrease of food consumption, of body weight development and organ weights, and a significant increase in SGOT and SGPT. Moreover, in rats of both sexes treated with levosulpiride at all tested doses a significant increase of plasma prolactin and a moderate increase of corticosterone and aldosterone were shown. Macroscopically and microscopically there were no signs of oncogenic properties with all the doses of levosulpiride tested. At histopathologic examinations benign neoplasms of skin (epithelial and connectival turnours), soft tissues (lipomas, angiomas, leiomiomas), thyroid gland (follicular adenomas), ovaries (thecagranulosa cell tumours), liver (adenomas) and adrenal medulla (phaeochromocytomas) were observed. Microscopic alterations of liver were observed only with the highest dose of levosulpiride (50.0 mg/kg/day). With levosulpiride at all doses tested microscopic aspect of hyperactivity of mammary and pituitary glands has been observed. Moreover, in control and treated rats of both sexes aspecific alterations of lungs, kidneys, heart, spleen and liver were documented. Similar results dropped out from the trials on mice by using the same doses of levosulpiride (12.5, 25.0 and 50.0 mg/kg/day in the food).
Reference
The oncogenic/carcinogenic toxicity of levosulpiride was tested in 600 Wistar rats and NMRI mice by long-term oral administration. 200 further rats and 200 further mice served as controls. Levosulpiride was given over 104 weeks in rats and 100 weeks in mice in daily dosage of 12.5, 25.0 and 50.0 mg/kg/day in the food. The control rats and mice remained untreated. The final mortality was significantly higher, in respect to controls, in rats and mice treated with levosulpiride at the dose of 50.0 mg/kg/day and it was similar or identic to controls in the groups treated with levosulpiride at doses of 12.5 and 25.0 mg/kg/day. The researches in rats showed that the lowest and medium tested dosage of levosulpiride (12.5 and 25.0 mg/kg/day in the food) were in the range of the estimated good tolerated doses and did not influence the behaviour, the external appearance, the faeces, the mortality, the food and drinking water consumption, the haematological and urinary profiles, the body weight development, the weight of examinated organs, sight, hearing, dentition and the number of palpable masses. The highest dose of levosulpiride (50.0 mg/kg/day in the food) did not modify the behaviour, the external appearance, faeces, the drinking water consumption, the haematological and urinary profiles, sight, hearing, dentition or the number of palpable masses, but it induced a significant decrease of food consumption, of body weight development and organ weights, and a significant increase in SGOT and SGPT. Moreover, in rats of both sexes treated with levosulpiride at all tested doses a significant increase of plasma prolactin and a moderate increase of corticosterone and aldosterone were shown. Macroscopically and microscopically there were no signs of oncogenic properties with all the doses of levosulpiride tested. At histopathologic examinations benign neoplasms of skin (epithelial and connectival turnours), soft tissues (lipomas, angiomas, leiomiomas), thyroid gland (follicular adenomas), ovaries (thecagranulosa cell tumours), liver (adenomas) and adrenal medulla (phaeochromocytomas) were observed. Microscopic alterations of liver were observed only with the highest dose of levosulpiride (50.0 mg/kg/day). With levosulpiride at all doses tested microscopic aspect of hyperactivity of mammary and pituitary glands has been observed. Moreover, in control and treated rats of both sexes aspecific alterations of lungs, kidneys, heart, spleen and liver were documented. Similar results dropped out from the trials on mice by using the same doses of levosulpiride (12.5, 25.0 and 50.0 mg/kg/day in the food).
Endpoint conclusion
- Quality of whole database:
- The quality of database is limited as the reliability of the studies cannot be assigned.
Carcinogenicity: via inhalation route
Endpoint conclusion
- Endpoint conclusion:
- no study available
Carcinogenicity: via dermal route
Endpoint conclusion
- Endpoint conclusion:
- no study available
Justification for classification or non-classification
Overall, data available are conclusive but not sufficient for classification.
Additional information
Information on Registered Substances comes from registration dossiers which have been assigned a registration number. The assignment of a registration number does however not guarantee that the information in the dossier is correct or that the dossier is compliant with Regulation (EC) No 1907/2006 (the REACH Regulation). This information has not been reviewed or verified by the Agency or any other authority. The content is subject to change without prior notice.
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