In reactions containing dual-phosphorylated p38α, Pexmetinib at 1.25 μM increased the rate of activation loop threonine dephosphorylation by the catalytic domain of WIP1 10-fold compared to the DMSO-treated control. In osteoclasts on bovine bone slices, in a design also including RANKL and M−CSF, Pexmetinib reduced resorption area by about 45% at 0.1 µM and about 88% at 0.4 μM compared to the control group without Pexmetinib. [1,2]
Literature-reported observations and conditions; not Adooq-tested protocols or general treatment recommendations.
Activation Loop Threonine Dephosphorylation in Dual-Phosphorylated p38α
Cell-based study · dual-phosphorylated p38α (p38α-2p) [1]
In reactions containing dual-phosphorylated p38α, Pexmetinib was added at 1.25 μM immediately before the reaction began. It increased the rate of pT180 dephosphorylation by the catalytic domain of WIP1 10-fold.
Literature-Reported Treatment Conditions
- Treatment concentration
- 1.25 μM
- Exposure duration
- immediately before the start of the reaction
- Method
- added to reactions
- Vehicle
- 5% final DMSO concentration
Methods and source locations
Compound reported in the paper: Pexmetinib
Literature evidence for the named compound in the stated model; no Adooq product-use or lot-performance claim.
Results > Conformation-Selective p38α MAP Kinase Inhibitors Modulate Threonine Dephosphorylation by WIP1. (S1, S3, S4); Methods > Phosphatase Assays. > WIP1 and PPM1A. (S127, S128, S131, S132); Fig. 1. legend (S160)
dephosphorylation of the activation loop threonine (pT180) by the catalytic domain of WIP1: dephosphorylation of the activation loop threonine (pT180) by the catalytic domain of WIP1; comparator: DMSO treated control — Results > Conformation-Selective p38α MAP Kinase Inhibitors Modulate Threonine Dephosphorylation by WIP1. (S3, S4)
Osteoclast Resorption of Bovine Bone Slices
Cell-based study · osteoclasts on the bovine bone slices [2]
Osteoclasts on bovine bone slices were treated with Pexmetinib. Compared to the control group, resorption area was reduced by about 45% at 0.1 µM and about 88% at 0.4 μM.
Literature-Reported Treatment Conditions
- Treatment concentration
- 0, 0.1, 0.2, 0.4 μM
- Exposure duration
- for another 3 days
- Vehicle
- DMSO
- Co-treatment
- Other interventions in this design: RANKL 50 ng/mL; M−CSF 25 ng/mL. Compound effect isolated by the comparison: compared to the control group.
- Reported limits
- Not stated in the sentences used: route.
Methods and source locations
Compound reported in the paper: Pexmetinib
Literature evidence for the named compound in the stated model; no Adooq product-use or lot-performance claim.
Materials and methods > Materials and main reagents (S8); Materials and methods > In vitro osteoclastogenesis (S25); Materials and methods > In vitro bone absorption assay of osteoclast (S50, S51, S53); Results > Pexmetinib inhibited RANKL-induced osteoclast formation in vitro (S95, S97)
resorption area of bovine bone slices: resorption area of bovine bone slices; comparator: without Pexmetinib — Materials and methods > In vitro bone absorption assay of osteoclast (S53); Results > Pexmetinib inhibited RANKL-induced osteoclast formation in vitro (S97)
