ML133 | Kir2 potassium channel blocker
Available Options
| Size: | Price | Quantity | |
|---|---|---|---|
| 5 mg | $50.00 | ||
| 25 mg | $150.00 |
ML133 (1222781-70-5) is a potent and selective blocker of the inwardly rectifying Kir2 potassium channel, IC50s = 1.8, 2.8, 2,9, and 4.0 µM for Kir2.1, Kir2.6, Kir2.2, and Kir2.3, respectively.1 Intrathecal injection of ML133 attenuated the proliferation of microglia and neuropathic pain behaviors after nerve injury.2 ML133 inhibits microglial priming pointing to Kir2.1 channels as a new therapeutic target for neuronal damage.3 Moreover, treatment with ML133 one hour post-injury was sufficient to improve neuronal survival in a traumatic brain injury human organoid model.4
References/Citations:
- Wang et al. (2011), Selective inhibition of the K(ir)2 family of inward rectifier potassium channels by a small molecule probe: the discovery, SAR, and pharmacological characterization of ML133; ACS Chem. Biol. 6 845
- Gattlen et al. (2020), The inhibition of Kir2.1 potassium channels depolarizes spinal microglial cells, reduces their proliferation, and attenuates neuropathic pain; Glia 68 2119
- Spencer et al. (2016), Mechanisms Underlying Interferon-γ-Induced Priming of Microglial Reactive Oxygen Species Production; PLoS One 11 e0162497
- Lai et al. (2024), KCNJ2 inhibition mitigates mechanical injury in a human brain organoid model of traumatic brain injury; Cell Stem Cell 31 519
C19H19NO·HCl
>98% HPLC
NMR: (Conforms)
Safety Data Sheet:
Product Data Sheet:
Materials provided by Focus Biomolecules are for laboratory research use only and are not intended for human or veterinary applications. Please note that we do not sell to individuals and that all orders placed by non-research organizations will incur a $20 restocking/refund fee
ML133 (1222781-70-5) is a potent and selective blocker of the inwardly rectifying Kir2 potassium channel, IC50s = 1.8, 2.8, 2,9, and 4.0 µM for Kir2.1, Kir2.6, Kir2.2, and Kir2.3, respectively.1 Intrathecal injection of ML133 attenuated the proliferation of microglia and neuropathic pain behaviors after nerve injury.2 ML133 inhibits microglial priming pointing to Kir2.1 channels as a new therapeutic target for neuronal damage.3 Moreover, treatment with ML133 one hour post-injury was sufficient to improve neuronal survival in a traumatic brain injury human organoid model.4
References/Citations:
- Wang et al. (2011), Selective inhibition of the K(ir)2 family of inward rectifier potassium channels by a small molecule probe: the discovery, SAR, and pharmacological characterization of ML133; ACS Chem. Biol. 6 845
- Gattlen et al. (2020), The inhibition of Kir2.1 potassium channels depolarizes spinal microglial cells, reduces their proliferation, and attenuates neuropathic pain; Glia 68 2119
- Spencer et al. (2016), Mechanisms Underlying Interferon-γ-Induced Priming of Microglial Reactive Oxygen Species Production; PLoS One 11 e0162497
- Lai et al. (2024), KCNJ2 inhibition mitigates mechanical injury in a human brain organoid model of traumatic brain injury; Cell Stem Cell 31 519
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Focus Biomolecules • Plymouth Meeting, PA USA • 1-855-FOCUS21
Focus Biomolecules
Plymouth Meeting, PA USA
1-855-FOCUS21
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