Cat. No.: HY-N15522

Bi-magnolignan

Bi-magnolignan is a novel orally active bisbenzofuran lignan natural product with anticancer activity. Bi-magnolignan indirectly activates TBK1, triggering mitophagy, while binding to BRD4 (K_d 9.80 μM) to inhibit bromodomain transcriptional function. Bi-magnolignan disrupts the G2/M DNA damage checkpoint, inhibits homologous recombination repair, and induces DNA double-strand breaks and tumor cell apoptosis. Bi-magnolignan inhibits the growth of HCT116 and 4T1 xenograft tumors. Bi-magnolignan can be used for research related to triple-negative breast cancer and colorectal cancer.

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

CAS No.: 2883117-61-9
Formula: C₃₆H₃₀O₆
Molecular Weight:558.62

Storage:

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

Data Sheet (311 KB)

Bi-magnolignan Chemical Structure

CAS No.: 2883117-61-9

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Use of MCE Products

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

Biological Activity
- Description
- IC₅₀ & Target
- Cellular Effect
- In Vitro
- Parmacokinetics
- In Vivo
Chemical Information
Purity & Documentation
References
Calculators
Help & FAQs
Classifications
Bioz

Biological Activity

Description

IC₅₀ & Target

^[2]^[1]

BRD4

9.8 nM (Kd)

Caspase 3

Caspase-9

PARP

All Epigenetic Reader Domain Isoforms :

All Caspase Isoforms :

All PARP Isoforms :

Cellular Effect

Cell Line	Type	Value	Description	References
HCT-116	IC50	2.9 μM	Antiproliferative activity against human HCT116 cells assessed as viability reduction after 48 hrs incubation by CCK8/SRB assay. Antiproliferative activity against human HCT116 cells assessed as viability reduction after 48 hrs incubation by CCK8/SRB assay.	36936845
D341 cell line	IC50	15.79 μM	Antiproliferative activity against human D341 Med cells assessed as viability reduction after 48 hrs incubation by CCK8/SRB assay. Antiproliferative activity against human D341 Med cells assessed as viability reduction after 48 hrs incubation by CCK8/SRB assay.	36936845
HCT-8	IC50	21 μM	Antiproliferative activity against human HCT8 cells assessed as viability reduction after 48 hrs incubation by CCK8/SRB assay. Antiproliferative activity against human HCT8 cells assessed as viability reduction after 48 hrs incubation by CCK8/SRB assay.	36936845
LoVo	IC50	23.6 μM	Antiproliferative activity against human LOVO cells assessed as viability reduction after 48 hrs incubation by CCK8/SRB assay. Antiproliferative activity against human LOVO cells assessed as viability reduction after 48 hrs incubation by CCK8/SRB assay.	36936845
HCT-116	IC50	3.2 μM	Antiproliferative activity against human HCT116 cells transduced with vector assessed as viability reduction after 48 hrs incubation by CCK8/SRB assay. Antiproliferative activity against human HCT116 cells transduced with vector assessed as viability reduction after 48 hrs incubation by CCK8/SRB assay.	36936845
HCT-116	IC50	6.9 μM	Antiproliferative activity against human HCT116 cells overexpressing BRD4 assessed as viability reduction after 48 hrs incubation by CCK8/SRB assay. Antiproliferative activity against human HCT116 cells overexpressing BRD4 assessed as viability reduction after 48 hrs incubation by CCK8/SRB assay.	36936845
D341 cell line	IC50	4.4 μM	Antiproliferative activity against human D341 Med cells transduced with vector assessed as viability reduction after 48 hrs incubation by CCK8/SRB assay. Antiproliferative activity against human D341 Med cells transduced with vector assessed as viability reduction after 48 hrs incubation by CCK8/SRB assay.	36936845
D341 cell line	IC50	7.9 μM	Antiproliferative activity against human D341 Med cells overexpressing BRD4 assessed as viability reduction after 48 hrs incubation by CCK8/SRB assay. Antiproliferative activity against human D341 Med cells overexpressing BRD4 assessed as viability reduction after 48 hrs incubation by CCK8/SRB assay.	36936845

In Vitro

Anti-cancerApoptosisAutophagyLysosomal MetabolismMitochondrial FunctionMitochondrial Oxidative PhosphorylationCell Cycle RegulationOthers

Anti-cancer

Bi-magnolignan (BM) (24 h) inhibits the proliferation of MDA-MB-231 and 4T1 TNBC cells^[1].
Bi-magnolignan exhibits antiproliferative activity against HCT116 cells (IC₅₀ = 2.9 μM) and D341 Med cells (IC₅₀ = 15.79 μM)^[2].
Bi-magnolignan (0-7.5 μM; 10 days) inhibits HCT116 colony formation, and pre-incubation with Q-VD-OPh (HY-12305) reduces this long-term toxicity^[2].

Anti-cancer

Apoptosis

Autophagy

Bi-magnolignan (2-20 μM; 24 h) induces apoptosis in MDA-MB-231 and 4T1 cells, increases cleaved caspase-3 and cleaved caspase-9, induces LC3-II accumulation and p62 reduction, and decreases mitochondrial protein expression^[1].

Anti-cancer

Autophagy

Lysosomal Metabolism

Bi-magnolignan (20 µM; 24 h) induces mitophagy in MDA-MB-231 cells^[1].

Anti-cancer

Autophagy

Mitochondrial Function

Lysosomal Metabolism

Bi-magnolignan (5-20 μM; 24 h)-induced mitochondrial depletion and changes in mitophagy markers are reversed by BX795 (HY-10514), and BX795 also attenuates p62 phosphorylation and LC3-II accumulation in MDA-MB-231 and 4T1 cells^[1].

Anti-cancer

Autophagy

Mitochondrial Function

Mitochondrial Oxidative Phosphorylation

Lysosomal Metabolism

Bi-magnolignan (20 µM (MDA-MB-231 TBK1^−/−); 8 µM (4T1 TBK1^−/−); 24 h)-induced changes in mitophagy markers require TBK1 in MDA-MB-231 and 4T1 cells^[1].

Anti-cancer

Mitochondrial Function

Bi-magnolignan (2-20 μM; 24 h) induces mitochondrial membrane potential depolarization, reduces mitochondrial mass, decreases mtDNA copy number, and lowers cellular ATP levels in MDA-MB-231 and 4T1 cells, as well as in TNBC cells^[1].

Apoptosis

Bi-magnolignan (2.5-12; 0-48 h) induces apoptosis in HCT116 and D341 Med cells, accompanied by increased cleaved caspase-3, cleaved caspase-9, and cleaved PARP; it selectively decreases MYC protein levels in HCT116 and D341 Med cells^[2].
Bi-magnolignan (5-6 μM; 48 h) induces cell death and DNA damage in HCT116 and D341 Med cells; BRD4 overexpression attenuates these effects, whereas MYC or RNase H1 overexpression does not rescue the BM effects^[2].

Apoptosis

Cell Cycle Regulation

Bi-magnolignan inhibits BRD4 transcriptional function in HCT116 cells, downregulates BRD4 target genes including MYC, and increases the HRD score^[2].

Others

Bi-magnolignan (BM) binds BRD4 with a K_d of 9.80 μM and increases the thermal stability of BRD4 in HCT116 lysates^[2].

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

Apoptosis Analysis^[1]

Cell Line:

MDA-MB-231 and 4T1 cells
Concentration:

MDA-MB-231: 0, 5, 10, 20 µM
4T1: 0, 2, 4, 8 µM
Incubation Time:

24 h
Result:

Induced apoptosis in MDA-MB-231 and 4T1 cells.

Western Blot Analysis^[1]

Cell Line:

MDA-MB-231 and 4T1 cells
Concentration:

MDA-MB-231: 0, 5, 10, 20 µM
4T1: 0, 2, 4, 8 µM
Incubation Time:

24 h
Result:

Increased cleaved caspase-3 and cleaved caspase-9 in MDA-MB-231 and 4T1 cells.
Increased LC3-II accumulation and p62 reduction in MDA-MB-231 and 4T1 cells.

Cell Autophagy Assay^[1]

Cell Line:

MDA-MB-231 cells
Concentration:

20 µM
Incubation Time:

24 h
Result:

Markedly increased red fluorescence, confirming the induction of mitophagy.

Real Time qPCR^[1]

Cell Line:

MDA-MB-231 and 4T1 cells
Concentration:

MDA-MB-231: 0, 5, 10, 20 µM
4T1: 0, 2, 4, 8 µM
Incubation Time:

24 h
Result:

mtDNA copy number was significantly decreased after BM exposure.

Western Blot Analysis^[1]

Cell Line:

MDA-MB-231 and 4T1 cells
Concentration:

MDA-MB-231: 0, 5, 10, 20 µM
4T1: 0, 2, 4, 8 µM
BX795 combination: MDA-MB-231 20 µM BM + 1 µM BX795; 4T1 8 µM BM + 0.5 µM BX795
Incubation Time:

24 h
Result:

Elevated TBK1 (Ser172) and p62 (Ser403) phosphorylation in a dose‑ and time‑dependent manner upon BM exposure.
Reversal of BM‑caused decreases in mtDNA copy number, mitochondrial mass, mt‑Keima degradation signal and mitochondrial protein loss was achieved via pharmacological TBK1 inhibition using BX795.
Attenuation of BM‑induced p62 phosphorylation and LC3‑II accumulation was also observed following BX795 treatment.

Western Blot Analysis^[1]

Cell Line:

MDA-MB-231 and 4T1 cells
Concentration:

20 µM BM (MDA-MB-231 TBK1^-/-); 8 µM BM (4T1 TBK1^-/-)
Incubation Time:

24 h
Result:

Loss of TBK1 mitigated BM-induced mitochondrial protein degradation, p62 phosphorylation and LC3-II accumulation.

Western Blot Analysis^[2]

Cell Line:

HCT116 and D341 Med cells
Concentration:

HCT116: 0, 2.5, 5, 7.5 µM (48 h)
HCT116: 5 µM (0-48 h)
D341: 0, 3, 6, 12 µM (48 h)
D341: 6 µM (0-48 h)
Incubation Time:

48 h
0, 6, 12, 24, 48 h
Result:

Induced apoptosis in HCT116 and D341 Med cells, accompanied by increased cleaved caspase-3, cleaved caspase-9, and cleaved PARP.
Decreased MYC protein levels in HCT116 and D341 Med cells.

Cell Proliferation Assay^[2]

Cell Line:

HCT116 cells
Concentration:

0 and 7.5 μM
Incubation Time:

10 days
Result:

Inhibited HCT116 colony formation, and pre-incubation with Q-VD-OPh (HY-12305) reduces this long-term toxicity.

Parmacokinetics

Species	Dose	Route	T_max	C_max	CL	V_d	AUC_0-∞	AUC_0-t
Mice^[2]	50 mg/kg	p.o.	1 h	3478.46 μg/L	23.931 L/h/kg	3.917 L/kg	5902.37 h·μg/L	5506.61 h·μg/L

In Vivo

Anti-cancer

Bi-magnolignan (BM) (50 mg/kg; p.o.; once every 48 hours; last dose on day 22 after implantation) inhibits 4T1 orthotopic tumor growth in female BALB/c mice^[1].
Bi-magnolignan (BM) (50 mg/kg; p.o.; once every 2 days) inhibits tumor growth in HCT116 xenograft nude mice^[2].

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

Animal Model:

BALB/c (female, 6-8 weeks old, received subcutaneous injection of 1 × 10⁵ 4T1 breast cancer cells)^[1]
Dosage:

50 mg/kg
Administration:

p.o.; once every 48 h; final dose on day 22 post-implantation
Result:

Revealed reduced tumor volumes in Bi‑magnolignan‑treated mice relative to vehicle controls by day 22 post‑implantation.
Demonstrated elevated phosphorylated TBK1 and decreased VDAC1 in tumor lysates of Bi‑magnolignan‑treated mice versus vehicle‑treated tumors.

Animal Model:

Athymic nude (4-6 weeks old, implanted in their hind limbs with 2,000,000 HCT116 cells suspended in 100 μL of PBS)^[2]
Dosage:

50 mg/kg
Administration:

p.o.; every 2 days
Result:

Resulted in tumor regression.
Exhibited increased levels of apoptosis marker cleaved‑PARP and DNA damage marker γH2AX, accompanied by reduced MYC expression in Bi‑magnolignan‑treated tumors.
Showed comparable body weight, normal physical activity and health status in mice from both groups throughout the study; detected no abnormalities during tissue collection.

Related Protocols :

Chemical Information

CAS No. 2883117-61-9
Molecular Weight 558.62
Formula C₃₆H₃₀O₆
SMILES

C=CCC1=C(O)C(O)=C(C2=C3C(OC4=C3C=C(CC=C)C=C4)=C(CC=C)C(O)=C2O)C5=C1OC6=CC=C(CC=C)C=C65
Structure Classification
- Phenols
- Polyphenols
Initial Source
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

Select Batch:

Purity: 99.98%

Assay: 99.98%

ee.: 99.98%

Data Sheet (311 KB)
COA (2659 KB)
Elemental Analysis Report (2659 KB)
HNMR (2659 KB)
CNMR (2659 KB)
RP-HPLC (2659 KB)
NP-HPLC (2659 KB)
MS (2659 KB)
LCMS (2659 KB)
IR (2659 KB)
GC (2659 KB)
OR (2659 KB)
SDS-PAGE (2659 KB)
SEC-HPLC (2659 KB)
Other Report (2659 KB)
Handling Instructions (2659 KB)

References

[1]. Chu T, et al. Bi-magnolignan suppresses triple-negative breast cancer by triggering TBK1-dependent mitophagy. Tissue & cell. 2026 Oct;102:103550. [Content Brief]

[2]. Huang Z, et al. Discovery of Bi-magnolignan as a novel BRD4 inhibitor inducing apoptosis and DNA damage for cancer therapy. Biochemical pharmacology. 2025 May;235:116843. [Content Brief]

[3]. Lu SY, et al. Total synthesis of bi-magnolignan. RSC advances. 2023 Mar 14;13(13):8844-8846.

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Help & FAQs

How should lyophilized recombinant proteins be reconstituted and stored?

1. Before opening the cap, centrifuge the vial at 13000 rpm for 20-30 seconds. This step will ensure that any lyophilized powder that may have adhered to the cap or walls is collected at the bottom of the vial, minimizing the risk of product loss.

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Bi-magnolignan

All Epigenetic Reader Domain Isoforms

All Caspase Isoforms

All PARP Isoforms