In LN229, U87MG and LNZ308 glioma cells, Adooq A10905 reduced MTS viability with concentration and exposure time. The reported 48-h IC50 values were 25.05, 170.83 and 318.13 µM, respectively. Sensitivity varied between models; these results do not establish that growth suppression depends on AT1 blockade. [3]
AT1-selective binding of BIBR 277
Biochemical assay · Rat lung (AT1) and adrenal-medulla (AT2) membrane preparations [1]
BIBR 277 displaced radiolabeled angiotensin II at lung AT1 sites. Adrenal-medulla binding was much weaker, and saturation experiments supported competitive binding.
Literature-Reported Treatment Conditions
- Treatment concentration
- Concentration-dependent competition; saturation experiments used 3 and 10 nM BIBR 277.
- Exposure duration
- 60 min at 37 °C
- Method
- [125I]-angiotensin II competition and saturation binding
- Vehicle
- Vehicle condition in saturation studies; composition not specified for binding
- Reported limits
- Binding solvent and confidence intervals were not specified in the selected methods/results.
Methods and source locations
Compound reported in the paper: Telmisartan; Compound label in the paper: BIBR 277
Compound-level evidence; no Adooq product or lot tested.
pp. 246, 248; Binding studies; Receptor binding studies; Figs. 2–3
Inhibition constant at rat lung AT1 sites: Competition binding; n = 3 experiments run in triplicate. Results are mean ± s.e.mean per Data analysis. — p. 248, Receptor binding studies; Fig. 2a
Inhibition constant at rat adrenal-medulla AT2 sites: [125I]-angiotensin II displacement; same Fig. 2 experimental replication statement. — p. 248, Receptor binding studies; Fig. 2b
Radioligand dissociation constant with increasing BIBR 277: Saturation binding; n = 4 experiments in duplicate; Bmax remained unchanged. Mean ± s.e.mean. — p. 248, Results and Fig. 3
PPARγ partial agonism in a transactivation assay
Cell-based study · CV-1 cells carrying a murine PPARγ ligand-binding-domain/GAL4 luciferase reporter and β-galactosidase internal control [2]
Telmisartan activated the PPARγ reporter with lower maximal efficacy than rosiglitazone or pioglitazone. High telmisartan concentrations attenuated activation by rosiglitazone in the mixing experiment.
Literature-Reported Treatment Conditions
- Treatment concentration
- Concentration-response series; 10 µmol/L ARB comparison and 40 µmol/L maximal-activation comparison; mixing arm used 1 µmol/L rosiglitazone.
- Exposure duration
- 24 h drug incubation, beginning 24 h after transfection
- Method
- Luciferase activity normalized to β-galactosidase
- Vehicle
- Reporter-assay vehicle not specified in this methods subsection
- Co-treatment
- Separate Fig. 1D mixing condition: 1 µmol/L rosiglitazone plus variable telmisartan. Potency and partial efficacy derive from single-agent conditions.
- Reported limits
- Assay solvent, biological-repeat count and EC50 uncertainty are not specified in the selected reporter description; treatments were in triplicate.
Methods and source locations
Compound reported in the paper: Telmisartan; Compound label in the paper: telmisartan
Reporter-system partial agonism; no clinical efficacy or direct binding conclusion.
Early-pagination PDF pp. 2–3; Experimental Compounds; PPAR Transactivation Assays; Results: Telmisartan Is a Partial Agonist of PPARγ; Fig. 1A–D
Half-maximal PPARγ reporter activation: Cell-based reporter activation; not a receptor-binding affinity or administered dose. — Early-pagination PDF p. 3, Results and Fig. 1C
Maximum activation relative to full agonists: Relative to pioglitazone/rosiglitazone full agonist maxima; reported text range, not an error estimate. — Early-pagination PDF p. 3, Results and Fig. 1B–C
Model-dependent suppression of glioma-cell viability
Cell-based study · Human LN229, U87MG and LNZ308 glioma cells [3]
Telmisartan lowered MTS viability with concentration and exposure time. Reported 48-h IC50 values differed markedly between lines. High AGTR1 expression did not identify the most sensitive line.
Literature-Reported Treatment Conditions
- Treatment concentration
- Fig. 2A: LN229, 0/25/50/100 µM; U87MG and LNZ308, 0/100/200/400 µM.
- Exposure duration
- 24, 48 and 72 h; IC50 values reported at 48 h
- Method
- MTS metabolic-viability assay, absorbance at 490 nm
- Vehicle
- DMSO control
- Co-treatment
- None
- Reported limits
- DMSO percentage, IC50 fitting details and confidence intervals not supplied in selected text. Serum description is internally inconsistent; not normalized here.
Methods and source locations
Compound reported in the paper: Telmisartan; Compound label in the paper: telmisartan (A10905, AdooQ)
In-vitro glioma viability evidence only; no clinical antitumor efficacy or AT1-dependent killing inferred.
Materials and methods: Chemicals, Cell culture and transfection, MTS cell viability assay, Statistical analysis; Results: Telmisartan as an effective anticancer agent for glioma; Fig. 2A
48-h MTS viability inhibition: Exact values are reported in Results, not read from curves. Three independent experiments in Methods; Fig. 2 n = 3, error bars ± SD. No uncertainty is supplied for these IC50 estimates. — Results: Telmisartan as an effective anticancer agent for glioma; Fig. 2A
