Cat. No.: HY-N20662

(+)-Neoalbaconol

(+)-Neoalbaconol is a selective Akt/PDK1 inhibitor (with an IC₅₀ of 10 μM against hPDK1). (+)-Neoalbaconol selectively inhibits cancer cell proliferation, and induces energy depletion, apoptosis, autophagy and necroptosis in cancer cells. In addition, (+)-Neoalbaconol downregulates cIAP1/2 and TRAFs to activate non-canonical NF-κB and promote TNFα transcription, blocks EGFR-mediated VEGF production and receptor activation, and mediates cell necrosis via the RIPK3-ROS-dependent pathway. (+)-Neoalbaconol can be used in research related to nasopharyngeal carcinoma, melanoma, breast cancer and gastric cancer.

For research use only. We do not sell to patients.

CAS No.: 2779545-15-0
Formula: C₂₂H₃₄O₃
Molecular Weight:346.50

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Please store the product under the recommended conditions in the Certificate of Analysis.

(+)-Neoalbaconol Chemical Structure

CAS No.: 2779545-15-0

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Strong Fluorescence Signal / Multi-Disciplinary Applications / High Fluorescence Specificity

Biological Activity
- Description
- Cellular Effect
- In Vitro
- In Vivo
Chemical Information
Purity & Documentation
References
Calculators
Help & FAQs
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Biological Activity

Description

All Akt Isoforms :

Cellular Effect

Cell Line	Type	Value	Description	References
HepG2	EC₅₀	11.09 μM Compound: 37	Antiproliferative activity against human HepG2 cells assessed as inhibition of cell proliferation incubated for 72 hrs by MTT assay Antiproliferative activity against human HepG2 cells assessed as inhibition of cell proliferation incubated for 72 hrs by MTT assay	[PMID: 34653771]
MCF7	EC₅₀	11.32 μM Compound: 37	Antiproliferative activity against human MCF7 cells assessed as inhibition of cell proliferation incubated for 72 hrs by MTT assay Antiproliferative activity against human MCF7 cells assessed as inhibition of cell proliferation incubated for 72 hrs by MTT assay	[PMID: 34653771]

In Vitro

(+)-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.

Cell Cytotoxicity Assay^[1]

Cell Line:

C666-1 nasopharyngeal carcinoma cells
Concentration:

5, 10, 20 μM
Incubation Time:

24 h; 48 h
Result:

Induced dose- and time-dependent cell death in C666-1 cells.
Reached cell death rates of ~7% at 5 μM, ~9% at 10 μM, and ~24% at 20 μM after 24 h.
Reached cell death rates of ~15% at 5 μM, ~19% at 10 μM, and ~32% at 20 μM after 48 h, with a statistically significant increase at 20 μM compared to control.

Apoptosis Analysis^[1]

Cell Line:

C666-1 nasopharyngeal carcinoma cells
Concentration:

40 μM (annexin V-FITC/PI staining)
Incubation Time:

24 h (annexin V-FITC/PI staining)
Result:

Increased the percentage of annexin V-positive C666-1 cells to 78.2% after 24 h of 40 μM treatment.
Induced cleavage of caspases and PARP-1, confirming activation of the apoptotic pathway.

Cell Autophagy Assay^[1]

Cell Line:

C666-1, HK1, CNE1 nasopharyngeal carcinoma cells
Concentration:

20, 30, 40 μM (LC3/p62 immunoblotting); 40 μM (YFP-LC3 confocal microscopy, autophagic flux assay)
Incubation Time:

8 h (LC3/p62 immunoblotting); 6 h (YFP-LC3 confocal microscopy)
Result:

Upregulated endogenous LC3-II protein levels and reduced p62 protein levels in C666-1 cells.
Induced punctate aggregation of YFP-LC3 fluorescence in C666-1 cells, indicating autophagosome formation.
Increased autophagic vacuoles in treated cells as revealed by transmission electron microscopy.
Cotreatment with bafilomycin further elevated LC3-II levels and attenuated p62 reduction, confirming active autophagic flux.

Western Blot Analysis^[1]

Cell Line:

C666-1, HK1 nasopharyngeal carcinoma cells
Concentration:

20, 30, 40 μM (8 h short-term pathway inhibition); 0.625, 1.25, 2.5, 5, 10 μM (5 days long-term low-dose inhibition); 40 μM (8 h metabolic regulator mRNA/protein analysis)
Incubation Time:

8 h (short-term pathway inhibition, metabolic regulator analysis); 5 days (long-term low-dose inhibition)
Result:

Suppressed phosphorylation of Akt at Ser308 and Ser473 without altering PDK1 phosphorylation, and dose-dependently inhibited phosphorylation of downstream molecules TSC2, mTOR, and p70S6K1.
Inhibited Akt and mTOR phosphorylation with long-term low-dose treatment.
Suppressed TNFα-, EGF-, IL6-, and FBS-induced Akt activation after preincubation.
Specifically downregulated HK2 mRNA and protein levels in C666-1 and HK1 cells.

Cell Viability Assay^[1]

Cell Line:

C666-1, HK1 nasopharyngeal carcinoma cells
Concentration:

40 μM (+)-Neoalbaconol; 40 μM necrostatin-1; 20 μM zVAD-fmk; 5 μM 3-MA; 50 μM SP600125
Incubation Time:

24 h; 1 h (SP600125 preincubation)
Result:

Inhibition of autophagy with 3-MA enhanced (+)-Neoalbaconol-induced cell death.
Inhibition of apoptosis with zVAD-fmk or necroptosis with necrostatin-1 rescued cell viability.
Cotreatment with SP600125 (JNK inhibitor) further increased (+)-Neoalbaconol-induced cell death.
Activated JNK phosphorylation; inhibitors of apoptosis, necroptosis, autophagy, or JNK did not cross-inhibit other pathways.

Real Time qPCR^[2]

Cell Line:

human nasopharyngeal carcinoma C666-1, HK1, CNE1-LMP1 cells, human breast cancer MX-1 cells, human gastric cancer AGS-EBV cells, human amelanotic melanoma A375 cells
Concentration:

40 μM (TNFα transcription, secretion analysis, viability assays with RIPK1 knockdown); 1, 2, 4 μg/mL neutralizing TNFα antibody (pre-treatment for viability assays)
Incubation Time:

8 h (TNFα transcription analysis); 0, 4, 8, 12 h (TNFα secretion analysis); 1 h neutralizing TNFα antibody pre-treatment; 48 h siRNA transfection prior to NA treatment
Result:

Induced a 3- to 15-fold increase of TNFα mRNA in NA-sensitive cell lines (C666-1, HK1, MX-1, AGS-EBV) after 8 h treatment, while NA-resistant cell lines (A375, CNE1-LMP1) showed less than a 2-fold induction.
Triggered TNFα secretion into culture medium over 12 h in NA-sensitive C666-1 and HK1 cells, while resistant CNE1-LMP1 cells showed low TNFα secretion.
Partially and dose-dependently rescued C666-1 and HK1 cells from induced death after pre-treatment with neutralizing TNFα antibody.
Blocked induced increases in TNFα mRNA and secretion after knockdown of RIPK1.

Western Blot Analysis^[2]

Cell Line:

human nasopharyngeal carcinoma C666-1, HK1 cells
Concentration:

20, 30, 40 μM (cIAP1/2, TRAF protein level analysis); 40 μM NA, 2 mM MG132 (proteasome inhibition assays); 40 μM NA (cIAP1/2 ubiquitination assays)
Incubation Time:

8 h (cIAP1/2, TRAF protein level analysis; cIAP1/2 ubiquitination assays); 1 h (proteasome inhibition assays); 48 h plasmid transfection prior to NA treatment
Result:

Reduced protein levels of cIAP1, cIAP2, XIAP, TRAF2, and TRAF6 in C666-1 and HK1 cells, but did not affect TRAF3, TRADD, or FADD levels.
Blocked NA-dependent decreases in cIAP1/2 protein levels after treatment with proteasome inhibitor MG132.
Enhanced auto-ubiquitination of cIAP1 and cIAP2.

Real Time qPCR^[2]

Cell Line:

human nasopharyngeal carcinoma C666-1 cells
Concentration:

40 μM NA, 40 μM NAI, 5 μM BAY11-7082 (TNFα transcription, viability assays); 40 μM NA (TNFα transcription, secretion analysis with IKKα knockdown); varying doses (viability assays with IKKα knockdown)
Incubation Time:

1 h inhibitor pre-treatment; 48 h siRNA transfection prior to NA treatment
Result:

Did not affect NA-induced TNFα transcription or cell death after treatment with canonical NF-κB pathway inhibitors (NAI, BAY11-7082).
Reduced NA-induced TNFα mRNA levels and secretion, and rescued C666-1 cells from NA-induced death after knockdown of IKKα.

Cell Proliferation Assay^[3]

Cell Line:

MDA-MB-231, MCF-7, MX-1, MCF-10A
Concentration:

6.25, 12.5, 25, 50 μM
Incubation Time:

72 h
Result:

Reduced cell viability by 82.06% in MDA-MB-231 cells, 45.22% in MCF-7 cells, and 78.12% in MX-1 cells at 50 μM.
Showed no toxic effect on MCF-10A cells at 50 μM.
Decreased viability of MDA-MB-231, MCF-7, and MX-1 cells in a dose-dependent manner across 6.25, 12.5, 25, 50 μM.
Maintained MCF-10A viability near baseline across 6.25, 12.5, 25, 50 μM.

Cell Proliferation Assay^[3]

Cell Line:

HUVECs
Concentration:

2.5, 5, 10 μM
Incubation Time:

24 h
Result:

Reduced VEGF-induced HUVEC viability by 21.02% at 10 μM.
Inhibited VEGF-induced proliferation in a dose-dependent manner across 2.5, 5, 10 μM.

Cell Migration Assay^[3]

Cell Line:

HUVECs
Concentration:

2.5, 5 μM
Incubation Time:

6 h
Result:

Reduced VEGF-induced migrated cell counts by 56.35% at 2.5 μM compared to VEGF-only controls.
Reduced VEGF-induced migrated cell counts by 83.26% at 5 μM compared to VEGF-only controls.
Inhibited VEGF-induced HUVEC migration in a dose-dependent manner.

Cell Invasion Assay^[3]

Cell Line:

HUVECs
Concentration:

2.5, 5 μM
Incubation Time:

30 min pretreatment, followed by 4-6 h incubation
Result:

Reduced VEGF-induced invasion by 60.33% at 2.5 μM compared to VEGF-only controls.
Reduced VEGF-induced invasion by 80.26% at 5 μM compared to VEGF-only controls.
Dramatically reduced VEGF-induced HUVEC invasiveness in a dose-dependent manner.

ELISA Assay^[3]

Cell Line:

MDA-MB-231
Concentration:

2.5, 5, 10, 20 μM (12 h incubation); 10 μM (4, 8, 12 h incubation)
Incubation Time:

4-12 h
Result:

Reduced VEGF levels by ~15% at 2.5 μM, ~35% at 5 μM, ~45% at 10 μM, and ~55% at 20 μM after 12 h incubation.
Reduced VEGF levels by ~30% at 4 h, ~40% at 8 h, and ~50% at 12 h at 10 μM.
Reduced VEGF secretion in dose- and time-dependent manners.

Western Blot Analysis^[3]

Cell Line:

MDA-MB-231
Concentration:

5, 10 μM
Incubation Time:

30 min pretreatment, followed by EGF stimulation
Result:

Inhibited EGF-induced phosphorylation of EGFR, Src, and STAT3 in a dose-dependent manner.
Achieved near-complete inhibition of p-EGFR at 10 μM.
Achieved partial inhibition of p-Src and p-STAT3 at 10 μM.
Left total protein levels of EGFR, Src, and STAT3 unchanged.

Western Blot Analysis^[3]

Cell Line:

HUVECs
Concentration:

5, 10 μM
Incubation Time:

30 min pretreatment, followed by VEGF stimulation
Result:

Inhibited VEGF-induced phosphorylation of VEGFR, EGFR, Src, and STAT3 in a dose-dependent manner.
Caused significant reduction in all phosphorylated proteins at 5 and 10 μM.
Left total protein levels of VEGFR, EGFR, Src, and STAT3 unchanged.

In Vivo

(+)-Neoalbaconol (100 mg/kg; daily; 30 days) reduces nasopharyngeal carcinoma xenograft tumor volume by 58.5% and tumor weight by 48.4% in BALB/c nu/nu nude mice via suppression of the PI3-K/Akt signaling pathway^[1].
(+)-Neoalbaconol (40 mg/kg; i.p.; daily; 15 days) reduces average breast cancer xenograft volume by 53% and weight by 64%, while decreasing tumor microvessel density by 75.68% and proliferation index by 57.82% in athymic nude mice^[3].
(+)-Neoalbaconol (2.5-5 μM; s.c.; single dose) reduces VEGF-induced microvessel formation by 69.20% and 84.62%, respectively, in C57BL/6 mice^[3].

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

Animal Model:

BALB/c nu/nu nude mice (male, 4- to 6-week-old, subcutaneously injected with 5×10⁶ C666-1 cells)^[1]
Dosage:

100 mg/kg
Administration:

daily
Result:

Reduced average tumor volume to 627 mm³ (vs. 1512 mm³ in vehicle controls), corresponding to a 58.5% reduction.
Reduced average tumor weight to 0.65 g (vs. 1.26 g in vehicle controls), corresponding to a 48.4% reduction.
Downregulated levels of phosphorylated mTOR, phosphorylated Akt, and HK2 in tumor tissue.
Caused slightly lower average body weight than controls with no evident signs of toxicity.

Animal Model:

athymic nude mice (5-week-old female)^[3]
Dosage:

40 mg/kg
Administration:

i.p.; daily; 15 days
Result:

Reduced average tumor volume to 420.53 mm³, compared to 894.79 mm³ in vehicle controls.
Reduced average tumor weight to 0.26 g, compared to 0.73 g in vehicle controls.
Decreased tumor microvessel density (CD31 staining) by 75.68% relative to vehicle controls.
Decreased Ki-67 proliferation index by 57.82% relative to vehicle controls.
Did not affect mouse body weight or cause pathological changes in liver, lung, kidneys, or spleen.

Animal Model:

C57BL/6 mice^[3]
Dosage:

2.5 μM; 5 μM
Administration:

s.c.; single dose
Result:

Decreased VEGF-induced microvessel number in Matrigel plugs by 69.20% at 2.5 μM relative to VEGF-only controls.
Decreased VEGF-induced microvessel number in Matrigel plugs by 84.62% at 5 μM relative to VEGF-only controls.

Chemical Information

CAS No. 2779545-15-0
Molecular Weight 346.50
Formula C₂₂H₃₄O₃
SMILES

C[C@@]12[C@H]([C@](O)(CC[C@@]1([H])C(C)(CCC2)C)C)CC3=C(C=C(C=C3O)O)C
Structure Classification
- Phenols
- Polyphenols
Initial Source
- Marine natural products
- Marine algae
Dictyopteris divaricata Okam
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.

Purity & Documentation

Handling Instructions (2659 KB)

References

[1]. Deng Q, et al. Neoalbaconol induces energy depletion and multiple cell death in cancer cells by targeting PDK1-PI3-K/Akt signaling pathway. Cell death & disease. 2013 Sep 19;4(9):e804. [Content Brief]

[2]. Yu X, et al. Neoalbaconol induces cell death through necroptosis by regulating RIPK-dependent autocrine TNFα and ROS production. Oncotarget. 2015 Feb 10;6(4):1995-2008. [Content Brief]

[3]. Yu X, et al. Neoalbaconol inhibits angiogenesis and tumor growth by suppressing EGFR-mediated VEGF production. Molecular carcinogenesis. 2017 May;56(5):1414-1426. [Content Brief]

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(+)-Neoalbaconol

All Akt Isoforms