PIK-III

A selective inhibitor of Vps34

此产品仅用于科学研究，我们不为任何个人用途提供产品和服务

库存: 现货

可选规格

包装

价格

促销价

数量
2mg

￥762.00

610.00

- +
5mg

￥1412.00

1130.00

- +
10mg

￥2287.00

1830.00

- +
25mg

￥5075.00

4060.00

- +
50mg

￥9062.00

7250.00

- +

已选 0 种 0 瓶

金额: ￥0.00

首页收藏

货号: ajci13600
CAS: 1383716-40-2
别名: Vacuolar Protein Sorting 34 Inhibitor 2, Vps34-IN2, Vps34 Inhibitor 2
分子式: C17H17N7
分子量: 319.36
纯度: >98%
溶解度: ≥ 31.9mg/mL in DMSO
储存: Store at -20°C
库存: 现货

Background

IC50: 18 nM for VPS34

PIK-III is a VPS34 inhibitor and is able to inhibit autophagy.

VPS34 kinase has been found to be responsible for synthesis and deposition of phosphatidylinositol-3-phosphate at autophagosome formation sites, resulting in the recruitment of PtdIns(3)P-binding proteins.

In vitro: In previous study, PIK-III was identified as a selective inhibitor of VPS34 binding in a hydrophobic pocket. In addition, PIK-III could acutely inhibit the autophagy and lipidation of LC3, which led to the stabilization of autophagy substrates. Moreover, substrates such as NCOA4 were identified by conducting ubiquitin-affinity proteomic assay on PIK-III-treated cells, which accumulated in cells with ATG7 deficience and co-localized with autolysosomes. NCOA4 could bind ferritin heavy chain-1 directly to target the iron-binding ferritin complex following starvation or iron depletion [1].

In vivo: Animal study showed that PIK-III-treated Ncoa4-/- mice had a profound accumulation of iron in splenic macrophages that were important for iron reutilization from engulfed red blood cells. In summary, such in vivo results provided a novel mechanism for selective autophagy of ferritin and revealed a previously untouched role for autophagy and NCOA4 in the control of in-vivo iron homeostasis [1].

Clinical trial: Up to now, PIK-III is still in the preclinical development stage.

Reference:
[1] Dowdle WE et al.? Selective VPS34 inhibitor blocks autophagy and uncovers a role for NCOA4 in ferritin degradation and iron homeostasis in vivo. Nat Cell Biol. 2014 Nov;16(11):1069-79.