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EIPA

CAS No. : 1154-25-2

MCE 国际站：EIPA

产品活性：EIPA (L593754) 是一种具有口服活性的 TRPP3 通道抑制剂，IC₅₀ 为 10.5 μM。EIPA 可通过抑制 Na⁺/H⁺-exchanger 3 (NHE3) 来促进自噬 (autophagy)。EIPA 也抑制巨胞饮作用 (macropinocytosis)。EIPA 可用于炎症和癌症的研究，如胃癌、结肠癌、胰腺癌。

研究领域：Membrane Transporter/Ion Channel  |  Neuronal Signaling  |  GPCR/G Protein  |  Autophagy  |  Immunology/Inflammation

作用靶点：TRP Channel  |  Prostaglandin Receptor  |  Autophagy  |  COX  |  Na+/H+ Exchanger (NHE)

In Vitro: EIPA (100 μM, 30 min) suppresses TRPP3-mediated Ca²⁺ uptake in X. laevis oocytes.
EIPA hydrochloride (10-100 μM) reversibly inhibits the basal Na⁺ current (IC₅₀: 19.5 μM).
EIPA (300 μM, 6h) enhances autophagy through NHE3 (Na⁺/H⁺-exchanger 3) in IEC-18 cells.
EIPA (20 μM, 2 h) blocks macropinocytosis-mediated uptake of CA-PZ massively entry in HT-29 cells and MIA PaCa-2 cells.
EIPA (30 μM, 3h) attenuates Zinc/Kainate toxicity by decreasing Zn²⁺ entry in cerebellar granule neurons.
EIPA (5-100 μM, 48h) suppresses proliferation of MKN28 cells through up-regulation of p21 expression.
EIPA (3 μM, 6 h) inhibits the LPS-induced increase in the level of COX-2 protein.

In Vivo: EIPA (Intravenous injection, 1 mg/kg) dose-dependently attenuates the I/R (Ischemia/reperfusion)-induced renal dysfunction in ddY strain mice.
EIPA (oral administration, 10 mg/kg) inhibits LPS-induced inflammation in air pouch-type LPS-induced inflammation model.

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