GTx-024 reduced cell numbers after six days in MDA-MB-231 breast-cancer cells engineered to overexpress AR. Bicalutamide did not inhibit growth in this experiment. The result is specific to this engineered model. [1]
In 24-hour myoblast experiments, ostarine increased BrdU incorporation at 1000 nM in C2C12 cells and at 1000–10,000 nM in L6 cells. MTT responses varied with model and concentration. These cellular findings do not establish whole-muscle hypertrophy. [2]
AR-dependent transcriptional activation
Cell-based study · Human MDA-MB-231 breast cancer cells transiently expressing human androgen receptor and GRE-luciferase reporter. [1]
GTx-024 acted as an AR agonist in this cellular reporter system. The inactive GTx-024R comparator lacked the reporter response seen with GTx-024; DHT was an active comparator. This is a functional transcriptional endpoint, not a binding constant.
Literature-Reported Treatment Conditions
- Treatment concentration
- Concentration-response series shown in Figure 1A (nM); Table 1 reports an AR-transactivation EC50 of 1 nM.
- Exposure duration
- Treatment 24 h after transfection; luciferase measured 48 h after transfection.
- Method
- AR-dependent GRE-luciferase reporter assay in MDA-MB-231 cells transfected with human AR and a renilla control.
- Co-treatment
- Comparator ligands were tested separately; no combination effect is claimed.
- Reported limits
- Treatment solvent not specified in the relevant transactivation methods. Renilla plasmid amounts differ between general methods and Figure 1A caption; these amounts are not reproduced here. Table 1 does not give an uncertainty for the reporter EC50.
Methods and source locations
Compound reported in the paper: Ostarine (enobosarm, GTx-024, MK-2866); Compound label in the paper: GTx-024
Applies to the named research compound in this reporter assay; no Adooq lot or enantiomeric-purity validation.
Figure 1A; Table 1 GTx-024 row; Methods: Transfection and transactivation assay; Statistical analysis
AR-dependent transactivation: GRE-luciferase with human AR; Table 1 reports EC50 without an uncertainty. nM context is supplied by the linked Figure 1A concentration axis. — Table 1, GTx-024 row and footnote; Figure 1A concentration axis
Growth response in an engineered AR-positive breast-cancer model
Cell-based study · Human MDA-MB-231 breast-cancer cells stably overexpressing wild-type AR (MDA-MB-231-AR). [1]
GTx-024 reduced cell numbers in the six-day experiment; DHT and GTx-027 also inhibited growth, whereas bicalutamide did not. This engineered model does not establish a response in all AR-positive or all triple-negative breast cancers.
Literature-Reported Treatment Conditions
- Treatment concentration
- 0.1, 1, 10, 100 and 1000 nM GTx-024, with a zero-concentration control (Figure 1E).
- Exposure duration
- 6 days
- Method
- Coulter-counter cell enumeration after treatment of MDA-MB-231 cells stably overexpressing AR.
- Co-treatment
- DHT, GTx-027 and bicalutamide were separate comparator treatments.
- Reported limits
- Treatment solvent and medium-renewal schedule for this six-day assay are not specified in the acquired relevant text. Numeric growth IC50 from Table 1 is not used because its assay cross-reference is ambiguous.
Methods and source locations
Compound reported in the paper: Ostarine (enobosarm, GTx-024, MK-2866); Compound label in the paper: GTx-024
Restricted to the AR-overexpressing MDA-MB-231 model and this six-day endpoint.
Figure 1E and caption; Results: AR agonists inhibit breast cancer cell proliferation; Methods: Cell culture and Statistical analysis
Cell number after six days: Direct cell counts; plotted means ± SE. General statistical methods report triplicate in vitro experiments; precise independent-repeat count for panel E is not separately identified. — Figure 1E and caption; Results paragraph beginning MDA-MB-231 cells were stably transfected
Proliferation and metabolic activity in two myoblast lines
Cell-based study · Mouse C2C12 and rat L6 myoblast cell lines from ECACC. [2]
After 24 h, ostarine increased BrdU incorporation at 1000 nM in C2C12 cells and at 1000 and 10,000 nM in L6 cells. MTT responses differed by cell line and concentration. MTT is a metabolic assay and does not alone establish increased cell survival.
Literature-Reported Treatment Conditions
- Treatment concentration
- 1, 10, 100, 1000 and 10,000 nM ostarine.
- Exposure duration
- 24 h; BrdU was present during the final 3 h.
- Method
- BrdU incorporation and MTT absorbance in serum-free experimental DMEM containing 0.2% BSA.
- Reported limits
- Treatment stock solvent is not specified in the read cell methods. DMSO is described for dissolution of MTT formazan after incubation, not as the treatment vehicle. Caption n = 9 combines n = 3 per group across 3 repetitions; independent biological replicate structure is not established.
Methods and source locations
Compound reported in the paper: Ostarine (enobosarm, GTx-024, MK-2866); Compound label in the paper: Ostarine
Named-compound results in cultured myoblasts; no equivalence to an Adooq batch, whole-muscle hypertrophy or clinical benefit.
Results 2.1; Figure 1A–D and caption; Methods 4.3, 4.4 and 4.6
BrdU incorporation: 24-h treatment; BrdU added after 21 h for 3 h. One-way ANOVA with Dunnett test; mean ± SEM, caption n = 9 (n = 3 per group, 3 repetitions). — Results 2.1; Figure 1A,C and caption; Methods 4.6
MTT absorbance: MTT after 24-h exposure; one-way ANOVA with Dunnett test; mean ± SEM, caption n = 9 (n = 3 per group, 3 repetitions). — Results 2.1; Figure 1B,D and caption; Methods 4.6
