SW-106
SW-106 is a selective antagonist of parathyroid hormone/parathyroid hormone-related peptide receptor (PPR) and PTHR1, with an IC50 value of 0.99 μM against PPR. SW-106 antagonizes cAMP responses. SW-106 can be used in the research of osteoporosis.
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- Formule: C17H16F5NO2
- Masse moléculaire:361.31
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Stockage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Activité biologique
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Chemical Information
- Protocole
- Pureté et documentation
- Références
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Help & FAQs
Activité biologique
Description
IC50 & Target
[1]|
PTH1R 0.99 μM (IC50) |
In Vitro
SW-106 (incubated for 3 h) competes with the PPR probe peptide DPC-AJ1951 for binding to PPR in B28 cells, with an IC50 of 0.99 μM, and does not act as an agonist to induce cAMP production in these cells[1].
SW-106 acts as a competitive antagonist of PPR-mediated cAMP production in B28, SaOS-2 and UMR106 cells, with an IC50 of 5.78 μM against DPC-AJ1951 and 68 μM against PTH-(1-34) in B28 cells[1].
SW-106 exhibits more selective activity toward PPR than toward the GLP-1 receptor and most tested class A GPCRs, showing only weak binding to a small subset of class A receptors at concentrations ≥10 μM[1].
SW-106 (3 × 10-5 M; up to 90 min) exhibits weak intrinsic agonist activity toward wild-type hPTHR1 expressed in GS-22A cells, increasing cAMP levels by ~5-fold at a concentration of 3 × 10-5 M[2].
SW-106 (1 × 10-6 M-1 × 10-5 M; up to 30 min) effectively inhibits the cAMP signaling pathway mediated by the tethered PTH (1-9) sequence on PTHR-Tether (1-9) expressed in GS-22A cells[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Chemical Information
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Masse moléculaire 361.31
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Formule C17H16F5NO2
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SMILES
O=C1NC2=CC=C(F)C(F)=C2[C@](C(F)(F)F)(/C=C/C3CC3)O[C@H]1CC
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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocole
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Research Protocol for Endocrine Diseases
Endocrine diseases often arise from disrupted hormone production, hormone signaling, or target-tissue responsiveness; for diabetes-focused endocrine disease models, insulin signaling regulates glucose uptake, hepatic glucose output, lipid metabolism, and β-cell compensation. Type 2 diabetes develops through interacting defects in insulin resistance, β-cell dysfunction, adipose inflammation, hepatic glucose overproduction, altered incretin signaling, and ectopic lipid metabolism. A major unresolved question is whether endocrine dysfunction is driven primarily by target-tissue insulin resistance, intrinsic β-cell failure, immune/inflammatory stress, or combined multi-organ failure that differs by disease stage.
Pureté et documentation
Références
[1]. Carter PH, et al. Discovery of a small molecule antagonist of the parathyroid hormone receptor by using an N-terminal parathyroid hormone peptide probe. Proc Natl Acad Sci U S A. 2007 Apr 17;104(16):6846-51. [Content Brief]
[2]. Carter PH, et al. Actions of the small molecule ligands SW106 and AH-3960 on the type-1 parathyroid hormone receptor. Mol Endocrinol. 2015;29(2):307-321. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
SW-106 Related Classifications
HY-113918 Related Classifications
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