HY-108618 Search Results


bc11 38  (MedChemExpress)
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MedChemExpress bc11 38
PDE11Ai’s across 3 scaffolds reverse aging-like PDE11A4 LLPS in hippocampal HT22 cells. Chemical structures for A) tadalafil, B) <t>BC11-38,</t> as well as C) MLG-199, MLG-185, MLG-122, SMQ-02-57, SMQ-03-30, and SMQ-03-20. Representative images of HT22 neuronal cells transfected with PDE11A4 and treated with either vehicle (left/top images) or a PDE11Ai (right/bottom images), along with quantification of the PDE11Ai’s ability to reverse aging-like PDE11A4 LLPS, shown for D) tadalafil, E) BC11-38, F) MLG-199, G) MLG-185, H) MLG-122, I) SMQ-02-57, J) SMQ-03-30, and K) SMQ-03-20. Differences in potency and efficacy here mirror differential effectiveness of these compounds in the catalytic assay (Table1; n=4 biological replicates/group). *vs. 0 μM, P<0.05-0.0001.
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PDE11Ai’s across 3 scaffolds reverse aging-like PDE11A4 LLPS in hippocampal HT22 cells. Chemical structures for A) tadalafil, B) BC11-38, as well as C) MLG-199, MLG-185, MLG-122, SMQ-02-57, SMQ-03-30, and SMQ-03-20. Representative images of HT22 neuronal cells transfected with PDE11A4 and treated with either vehicle (left/top images) or a PDE11Ai (right/bottom images), along with quantification of the PDE11Ai’s ability to reverse aging-like PDE11A4 LLPS, shown for D) tadalafil, E) BC11-38, F) MLG-199, G) MLG-185, H) MLG-122, I) SMQ-02-57, J) SMQ-03-30, and K) SMQ-03-20. Differences in potency and efficacy here mirror differential effectiveness of these compounds in the catalytic assay (Table1; n=4 biological replicates/group). *vs. 0 μM, P<0.05-0.0001.

Journal: bioRxiv

Article Title: Molecular mechanisms regulating PDE11A4 age-related liquid-liquid phase separation (LLPS) and its reversal by selective, potent and orally-available PDE11A4 small molecule inhibitors both in vitro and in vivo

doi: 10.1101/2025.05.20.654583

Figure Lengend Snippet: PDE11Ai’s across 3 scaffolds reverse aging-like PDE11A4 LLPS in hippocampal HT22 cells. Chemical structures for A) tadalafil, B) BC11-38, as well as C) MLG-199, MLG-185, MLG-122, SMQ-02-57, SMQ-03-30, and SMQ-03-20. Representative images of HT22 neuronal cells transfected with PDE11A4 and treated with either vehicle (left/top images) or a PDE11Ai (right/bottom images), along with quantification of the PDE11Ai’s ability to reverse aging-like PDE11A4 LLPS, shown for D) tadalafil, E) BC11-38, F) MLG-199, G) MLG-185, H) MLG-122, I) SMQ-02-57, J) SMQ-03-30, and K) SMQ-03-20. Differences in potency and efficacy here mirror differential effectiveness of these compounds in the catalytic assay (Table1; n=4 biological replicates/group). *vs. 0 μM, P<0.05-0.0001.

Article Snippet: Tadalafil (Tocris, 6311), BC11-38 (medchem express, Hy108618), rolipram (Sigma, R6520), and papaverine (Sigma, P3510) were obtained from commercial vendors.

Techniques: Transfection

The ability of PDE11Ai’s to reverse PDE11A4 LLPS was unaffected by A) preventing phosphorylation at S163, or B) preventing phosphorylation of at S239. Although introducing the A499D mutation that stabilizes PDE11A4 homodimerization did not completely block the ability of C) BC11-38 and D) SMQ-02-57 to reduce PDE11A4 LLPS, E) it did reduce the effectiveness of PDE11Ai’s across 6 experiments. F) Further, the ability of the A499D mutant to increase PDE11A4 LLPS in this series was ∼3-fold greater in the inhibitor-treated vs. vehicle-treated cells. Next we assessed the therapeutic potential PDE11Ai’s by determining if they could reverse the increased PDE11A4 LLPS caused by G) the aging-related S117D/S124D mutant,H) staurosporine, or the overexpression of the trans-Golgi network proteins I) TGN-38 (a.k.a. TGOLN1) and J) RhoB. In each experiment, PDE11Ai’s completely blocked the effects of the pro-LLPS manipulations. Post hoc: *vs. vehicle, P=0.0145-0.0001; #vs. WT, mCherry, or 0 µM staurosporine, P=0.0465-0.0001.

Journal: bioRxiv

Article Title: Molecular mechanisms regulating PDE11A4 age-related liquid-liquid phase separation (LLPS) and its reversal by selective, potent and orally-available PDE11A4 small molecule inhibitors both in vitro and in vivo

doi: 10.1101/2025.05.20.654583

Figure Lengend Snippet: The ability of PDE11Ai’s to reverse PDE11A4 LLPS was unaffected by A) preventing phosphorylation at S163, or B) preventing phosphorylation of at S239. Although introducing the A499D mutation that stabilizes PDE11A4 homodimerization did not completely block the ability of C) BC11-38 and D) SMQ-02-57 to reduce PDE11A4 LLPS, E) it did reduce the effectiveness of PDE11Ai’s across 6 experiments. F) Further, the ability of the A499D mutant to increase PDE11A4 LLPS in this series was ∼3-fold greater in the inhibitor-treated vs. vehicle-treated cells. Next we assessed the therapeutic potential PDE11Ai’s by determining if they could reverse the increased PDE11A4 LLPS caused by G) the aging-related S117D/S124D mutant,H) staurosporine, or the overexpression of the trans-Golgi network proteins I) TGN-38 (a.k.a. TGOLN1) and J) RhoB. In each experiment, PDE11Ai’s completely blocked the effects of the pro-LLPS manipulations. Post hoc: *vs. vehicle, P=0.0145-0.0001; #vs. WT, mCherry, or 0 µM staurosporine, P=0.0465-0.0001.

Article Snippet: Tadalafil (Tocris, 6311), BC11-38 (medchem express, Hy108618), rolipram (Sigma, R6520), and papaverine (Sigma, P3510) were obtained from commercial vendors.

Techniques: Phospho-proteomics, Mutagenesis, Blocking Assay, Over Expression