PAP-1 activity is model-dependent. At 2 µM, PAP-1 did not significantly reduce ATP- or silica-stimulated IL-1β release from primed primary mouse macrophages in the reported assay. [2]
In isolated mouse white adipocytes without insulin, PAP-1 increased glucose uptake at 1–3 µM, while 300 nM and lower tested concentrations had no significant effect. The authors questioned attribution of this metabolic response to Kv1.3 and proposed Kv1.5 involvement as a possibility. [3]
Competition with established inner-pore blockers
Cell-based study · L929 cells expressing human Kv1.3; whole-cell patch clamp at room temperature [1]
PAP-1 produced less additional current inhibition when intracellular TEA or extracellular verapamil was present, supporting an overlapping inner-pore blocking site.
Literature-Reported Treatment Conditions
- Treatment concentration
- 10 nM PAP-1
- Exposure duration
- Until steady-state block
- Method
- Bath application; internal TEA in pipette or external verapamil in bath
- Co-treatment
- 1 mM intracellular TEA or 20 µM extracellular verapamil in separate competition conditions
- Reported limits
- PAP-1 stock vehicle, exact exposure time and the error statistic for these percentages were not specified in the checked experiment text.
Methods and source locations
Compound reported in the paper: PAP-1 (5-(4-phenoxybutoxy)psoralen); Compound label in the paper: PAP-1
Evidence applies to the paper’s PAP-1 material and tested model. It does not validate an Adooq lot or establish clinical efficacy.
Figure 1A and Results: PAP-1 Competes with the Pore Blockers TEA and Verapamil; Methods: Patch-Clamp Experiments
Steady-state Kv1.3 current inhibition by 10 nM PAP-1: Whole-cell patch clamp; comparison of PAP-1 alone with sequential/co-applied pore blockers — Figure 1A and Results: PAP-1 Competes with the Pore Blockers TEA and Verapamil; Methods: Patch-Clamp Experiments
No detected inhibition of stimulated macrophage IL-1β release
Cell-based study · LPS-primed primary mouse bone-marrow-derived macrophages (pBMDMs) [2]
PAP-1 at 2 µM did not significantly change IL-1β release after ATP or silica stimulation under the tested conditions, while the NLRP3 inhibitor MCC950 provided an inhibitory positive control.
Literature-Reported Treatment Conditions
- Treatment concentration
- 2 µM PAP-1
- Exposure duration
- 15 min pretreatment before ATP (1 h) or silica (4 h) challenge
- Method
- Drug added after LPS priming; separate ATP- and silica-stimulated conditions
- Vehicle
- 1% (vol/vol) DMSO
- Co-treatment
- ATP or silica stimulation; MCC950 evaluated in a separate comparator condition
- Reported limits
- No exact numerical PAP-1 effect size or equivalence margin reported in the selected text; a nonsignificant result does not establish equivalence.
Methods and source locations
Compound reported in the paper: PAP-1 (5-(4-phenoxybutoxy)psoralen); Compound label in the paper: PAP-1
Evidence applies to the paper’s PAP-1 material and tested model. It does not validate an Adooq lot or establish clinical efficacy.
Figure 1ai–ii; Results section 3.2; Methods sections 2.1, 2.3 and 2.12
Supernatant IL-1β by ELISA: IL-1β ELISA; vehicle-stimulated control and MCC950 positive control — Figure 1ai–ii; Results section 3.2; Methods sections 2.1, 2.3 and 2.12
Micromolar glucose-uptake response with a lower-concentration negative result
Cell-based study · Isolated parametrial white adipocytes from female wild-type C57Bl6 mice; no insulin in this concentration-response experiment [3]
Glucose uptake increased significantly at 1 and 3 µM PAP-1 but not at 300 nM or lower tested concentrations. The authors questioned direct attribution to Kv1.3 and proposed Kv1.5 as a possible alternative.
Literature-Reported Treatment Conditions
- Treatment concentration
- 0, 3, 10, 30, 100, 300, 1000 and 3000 nM PAP-1
- Exposure duration
- 1 h
- Method
- Incubation of isolated adipocytes; extracellular-space correction with radiolabeled sucrose
- Co-treatment
- No insulin in the selected Figure 3 experiment
- Reported limits
- PAP-1 stock solvent/vehicle not specified in the retrieved Materials or adipocyte assay methods. Exact uptake values were not read from bar heights.
Methods and source locations
Compound reported in the paper: PAP-1 (5-(4-phenoxybutoxy)psoralen); Compound label in the paper: PAP-1
Evidence applies to the paper’s PAP-1 material and tested model. It does not validate an Adooq lot or establish clinical efficacy.
Figure 3; Methods: Materials, Glucose uptake by adipocytes, Statistical analysis; Results: Glucose uptake in Adipocytes; Discussion
Radiolabeled D-glucose uptake in the absence of insulin: D-[U-14C]glucose uptake over 1 h at 37°C; one-way ANOVA followed by Fisher least significant difference test — Figure 3; Methods: Materials, Glucose uptake by adipocytes, Statistical analysis; Results: Glucose uptake in Adipocytes; Discussion
