product name Betaxolol HCl
Description: Betaxolol HCl (also known as SL 75212 HCl) is a β1 adrenergic receptor blocker with IC50 of 6 μM. Betaxolol is able to protect retinal neurones. Betaxolol attenuates the NMDA-induced influx of 45Ca2+ while β-adrenoreceptor agonists are ineffective. The glutamate-induced release of LDH is almost completely prevented when betaxolol (10 μM) is included. Betaxolol (100 μM) is very effective in preventing the hypoxia-induced release of LDH from cortical cultures
References: Exp Eye Res. 2003 Apr;76(4):505-16; Exp Eye Res. 1999 Sep;69(3):331-42.
343.89
Formula
C18H29NO3.HCl
CAS No.
63659-19-8
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 69 mg/mL (200.6 mM)
Water: 69 mg/mL (200.6 mM)
Ethanol:
Solubility (In vivo)
Saline: 30 mg/mL
Synonyms
SL 75212 HCl
other peoduct :References PubMed ID：:http://www.ncbi.nlm.nih.gov/pubmed/19397803
| In Vitro |
In vitro activity: Betaxolol is able to protect retinal neurons. Betaxolol attenuates the NMDA-induced influx of 45Ca2+ while β-adrenoreceptor agonists are ineffective. The glutamate-induced release of LDH is almost completely prevented when betaxolol (10 μM) is included. Betaxolol (100 μM) is very effective in preventing the hypoxia-induced release of LDH from cortical cultures. Kinase Assay: Cell Assay: Dissociated cortical cells from 16–18-day-old fetal rats are grown, in 35 mm dishes, in DMEM supplemented with L-glutamine (4 mM), glucose (6 g/L), penicillin (100 U/mL), streptomycin (100 μg/mL) and 10% hormonal supplemented medium consisting of transferrin (1 mg/mL), insulin (250 μg/mL) putrescine (600 μM), sodium selenite (0.3 μM), progesterone (0.2 μM) and estradiol (0.1 pM) for 7 days in an atmosphere of 5% CO2/95% O2 at 37 °C. The cultures are then transferred to a culture medium which lacks the hormonal supplemented medium. L-glutamate is added to the medium and incubated for a further 4 hours under normoxic conditions. Betaxolol are added to the cultures at the same time as L-glutamate. In other experiments the cultures are subjected to anoxic conditions, 95% N2/5% CO2, for 5 hours at 37 °C. Betaxolol is added prior to anoxia. Reoxygenation is then achieved by replacing the cells in normoxic conditions (95% O2/5% CO2) for 3 hours. Cellular injury is assessed by measuring lactate dehydrogenase (LDH) release into the cell culture supernatant after hypoxia/reoxygenation or glutamate exposure. LDH activity is assayed spectrophotometrically by following NADH metabolism for 2 minutes at 340 nm. |
|---|---|
| In Vivo | When Betaxolol is injected i.p. into the rats before ischaemia and on the days of reperfusion the changes to the calretinin and ChAT immunoreactivities are reduced and the reduction of the b-wave is prevented. Inclusion of betaxolol partially prevents the changes caused by NMDA and lack of oxygen/glucose. |
| Animal model | Rat with ischemia model |
| Formulation & Dosage | Dissolved in saline; 2.5 mg/kg; i.p. injection |
| References | Exp Eye Res. 2003 Apr;76(4):505-16; Exp Eye Res. 1999 Sep;69(3):331-42. |
Related Posts
product name Betaxolol HCl
Description: Betaxolol HCl (also known as SL 75212 HCl) is a β1 adrenergic receptor blocker with IC50 of 6 μM. Betaxolol is able to protect retinal neurones. Betaxolol attenuates the NMDA-induced influx of 45Ca2+ while β-adrenoreceptor agonists are ineffective. The glutamate-induced release of LDH is almost completely prevented when betaxolol (10 μM) is included. Betaxolol (100 μM) is very effective in preventing the hypoxia-induced release of LDH from cortical cultures
References: Exp Eye Res. 2003 Apr;76(4):505-16; Exp Eye Res. 1999 Sep;69(3):331-42.
343.89
Formula
C18H29NO3.HCl
CAS No.
63659-19-8
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 69 mg/mL (200.6 mM)
Water: 69 mg/mL (200.6 mM)
Ethanol:
Solubility (In vivo)
Saline: 30 mg/mL
Synonyms
SL 75212 HCl
other peoduct :References PubMed ID：:http://www.ncbi.nlm.nih.gov/pubmed/19397803
| In Vitro |
In vitro activity: Betaxolol is able to protect retinal neurons. Betaxolol attenuates the NMDA-induced influx of 45Ca2+ while β-adrenoreceptor agonists are ineffective. The glutamate-induced release of LDH is almost completely prevented when betaxolol (10 μM) is included. Betaxolol (100 μM) is very effective in preventing the hypoxia-induced release of LDH from cortical cultures. Kinase Assay: Cell Assay: Dissociated cortical cells from 16–18-day-old fetal rats are grown, in 35 mm dishes, in DMEM supplemented with L-glutamine (4 mM), glucose (6 g/L), penicillin (100 U/mL), streptomycin (100 μg/mL) and 10% hormonal supplemented medium consisting of transferrin (1 mg/mL), insulin (250 μg/mL) putrescine (600 μM), sodium selenite (0.3 μM), progesterone (0.2 μM) and estradiol (0.1 pM) for 7 days in an atmosphere of 5% CO2/95% O2 at 37 °C. The cultures are then transferred to a culture medium which lacks the hormonal supplemented medium. L-glutamate is added to the medium and incubated for a further 4 hours under normoxic conditions. Betaxolol are added to the cultures at the same time as L-glutamate. In other experiments the cultures are subjected to anoxic conditions, 95% N2/5% CO2, for 5 hours at 37 °C. Betaxolol is added prior to anoxia. Reoxygenation is then achieved by replacing the cells in normoxic conditions (95% O2/5% CO2) for 3 hours. Cellular injury is assessed by measuring lactate dehydrogenase (LDH) release into the cell culture supernatant after hypoxia/reoxygenation or glutamate exposure. LDH activity is assayed spectrophotometrically by following NADH metabolism for 2 minutes at 340 nm. |
|---|---|
| In Vivo | When Betaxolol is injected i.p. into the rats before ischaemia and on the days of reperfusion the changes to the calretinin and ChAT immunoreactivities are reduced and the reduction of the b-wave is prevented. Inclusion of betaxolol partially prevents the changes caused by NMDA and lack of oxygen/glucose. |
| Animal model | Rat with ischemia model |
| Formulation & Dosage | Dissolved in saline; 2.5 mg/kg; i.p. injection |
| References | Exp Eye Res. 2003 Apr;76(4):505-16; Exp Eye Res. 1999 Sep;69(3):331-42. |