(+)-Neoalbaconol

(+)-Neoalbaconol (20-100 μM) dose-dependently inhibits PDK1 kinase activity, with near-complete inhibition at 100 μM^[1].
(+)-Neoalbaconol (50 μM; 7.5-18 μM IC₅₀ range) selectively inhibits proliferation of diverse cancer cell lines, with highest potency against C666-1 (IC₅₀ ~10 μM), HK1 (IC₅₀ ~18 μM), and ZR-75-1 (IC₅₀ ~7.5 μM) cells, and no effect on normal immortalized cell lines at 50 μM^[1].
(+)-Neoalbaconol (40 μM) induces necroptosis in C666-1 and HK1 cells, characterized by necrotic morphology, increased RIP1/RIP3 interaction, and viability rescue by necrostatin-1^[1].
(+)-Neoalbaconol (0.625-40 μM; 8 h-5 days) targets PDK1 to inhibit the PI3-K/Akt pathway and its downstream metabolic regulator HK2 in C666-1 and HK1 cells, suppressing Akt phosphorylation and downstream signaling, and reducing HK2 expression^[1].
(+)-Neoalbaconol (40 μM; 4-24 h) inhibits glucose consumption and ATP generation in C666-1 cells, with ATP depletion driving cell death that is partially rescued by Akt overexpression^[1].
(+)-Neoalbaconol (6.25-50 μM; 72 h) dose-dependently inhibits the viability of MDA-MB-231, MCF-7, and MX-1 human breast cancer cells in vitro (reducing viability by up to 82.06% at 50 μM) without affecting non-cancerous MCF-10A breast epithelial cells^[3].
(+)-Neoalbaconol (2.5-20 μM; 2 week) dose-dependently inhibits anchorage-independent colony formation of MDA-MB-231 human breast cancer cells in vitro, reducing colony counts by up to ~80% at 20 μM over 2 weeks^[3].
(+)-Neoalbaconol (2.5-10 μM; 24 h) inhibits VEGF-induced proliferation of HUVECs in vitro, reducing viability by 21.02% at 10 μM after 24 h^[3].
(+)-Neoalbaconol (2.5-5 μM; 6 h) dose-dependently inhibits VEGF-induced migration of HUVECs in vitro, reducing migrated cell counts by 56.35% at 2.5 μM and 83.26% at 5 μM after 6 h^[3].
(+)-Neoalbaconol (2.5-5 μM; 30 min pretreatment, followed by 4-6 h incubation) dose-dependently inhibits VEGF-induced invasion of HUVECs in vitro, reducing invasive cell counts by 60.33% at 2.5 μM and 80.26% at 5 μM after 4-6 h^[3].
(+)-Neoalbaconol (2.5-5 μM; 6-8 h) dose-dependently inhibits VEGF-induced capillary tube formation of HUVECs in vitro, reducing tube counts by 82.21% at 2.5 μM and 92.04% at 5 μM after 6-8 h^[3].
(+)-Neoalbaconol (2.5-20 μM; 4-12 h) dose- and time-dependently reduces VEGF secretion by MDA-MB-231 human breast cancer cells in vitro, decreasing VEGF levels by up to ~55% at 20 μM after 12 h^[3].
(+)-Neoalbaconol (5-10 μM; 30 min pretreatment, followed by VEGF stimulation) dose-dependently inhibits VEGF-induced activation of the VEGFR/EGFR/Src/STAT3 signaling pathway in HUVECs in vitro, reducing p-VEGFR, p-EGFR, p-Src, and p-STAT3 levels at 5 and 10 μM^[3].
(+)-Neoalbaconol (5-20 μM; 24-48 h) induces dose- and time-dependent cell death in C666-1 cells, reaching ~32% cell death at 20 μM over 48 h^[1].
(+)-Neoalbaconol (40 μM; 24 h) induces apoptosis in C666-1 cells, with 78.2% of cells staining positive for annexin V, and activation of caspase and PARP-1 cleavage^[1].
(+)-Neoalbaconol (20-40 μM; 6-8 h) induces active autophagy in C666-1, HK1, and CNE1 cells, as shown by LC3-II upregulation, p62 degradation, YFP-LC3 puncta formation, and confirmed autophagic flux^[1].
(+)-Neoalbaconol (20-40 μM; 0-24 h) induces RIPK1- and RIPK3-dependent necroptotic cell death in C666-1 and HK1 human nasopharyngeal carcinoma cells, as evidenced by MLKL phosphorylation, progressive membrane integrity loss, and reduced cell death with RIPK knockdown^[2].
(+)-Neoalbaconol (20-40 μM; 1, 8 h) triggers auto-ubiquitination and subsequent proteasomal degradation of cIAP1 and cIAP2, and reduces protein levels of TRAF2 and TRAF6, in C666-1 and HK1 human nasopharyngeal carcinoma cells^[2].
(+)-Neoalbaconol (0-40 μM; 8, 24 h) reduces K63-linked ubiquitination of RIPK1, inhibits the canonical NF-κB pathway, and activates the non-canonical NF-κB pathway in C666-1 human nasopharyngeal carcinoma cells^[2].
(+)-Neoalbaconol (40 μM; 24 h) induces independent apoptotic, necroptotic, and autophagic pathways in C666-1 and HK1 cells, with autophagy acting as a survival mechanism, and apoptosis/necroptosis driving cell death^[1].
(+)-Neoalbaconol (40 μM; 0-12 h, 48 h) induces autocrine TNFα production in NA-sensitive cancer cell lines (C666-1, HK1, MX-1, AGS-EBV) in a RIPK1-dependent manner, and autocrine TNFα contributes to NA-induced necroptotic cell death^[2].
(+)-Neoalbaconol (40 μM; 1, 48 h) relies on the non-canonical NF-κB pathway (mediated by IKKα) for induced TNFα production and necroptotic cell death in C666-1 human nasopharyngeal carcinoma cells, while the canonical NF-κB pathway is not involved^[2].
(+)-Neoalbaconol (40 μM; 12, 24 h) induces RIPK3-dependent ROS production originating from mitochondrial complex I, which contributes to necroptotic cell death in C666-1 human nasopharyngeal carcinoma cells^[2].
(+)-Neoalbaconol (20 μM) induces apoptosis in MDA-MB-231 and MX-1 human breast cancer cells in vitro, reducing viable cell counts by 21.55% and 30.08% respectively at 20 μM^[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.