6-Methoxydihydrosanguinarine hydrochloride 

6-Methoxydihydrosanguinarine hydrochloride is an alkaloid with activity across multiple cancer cell types. 6-Methoxydihydrosanguinarine hydrochloride activates IRE1/JNK signaling, blocks Akt/mTOR and PI3K/AKT/mTOR pathways, reduces expression of Cdc25C, CyclinB1, Cdc2, YAP/TAZ, Survivin, GPX4, and EGFR, upregulates IRE1 and DR5, and activates JNK and caspases. 6-Methoxydihydrosanguinarine hydrochloride induces apoptosis, G2/M phase arrest, DNA damage, ROS generation, lipid peroxidation, ferroptosis, autophagy, and suppresses cancer cell growth. 6-Methoxydihydrosanguinarine hydrochloride disruptes the biofilm formation of Candida albicans (C. albicans). 6-Methoxydihydrosanguinarine hydrochloride can be used for the research of non-small cell lung cancer, hepatocellular carcinoma, melanoma, colon carcinoma, ovarian cancer and breast cancer^{[1][2][3][4][5][6][7]}.

6-Methoxydihydrosanguinarine (0.15625-10 μM; 24 h) hydrochloride suppresses the viability of A549 and H1299 NSCLC cells in a dose-dependent manner, with IC₅₀ values of 2.154 μM and 2.586 μM respectively after 24 h treatment^[1].
6-Methoxydihydrosanguinarine (0.5-2 μM; 24 h) hydrochloride induces G2/M phase arrest in A549 and H1299 NSCLC cells after 24 h treatment at 2 μM, and G1 phase arrest in H1299 cells at lower concentrations^[1].
6-Methoxydihydrosanguinarine (0.5-2 μM; 24 h) hydrochloride downregulates cell cycle-related proteins Cdc25C, p-Cdc25C, cyclinB1, and Cdc2 in A549 and H1299 NSCLC cells after 24 h treatment^[1].
6-Methoxydihydrosanguinarine (0.5-2 μM; 24 h) hydrochloride dose-dependently activates the caspase cascade and induces PARP cleavage in A549 and H1299 NSCLC cells after 24 h treatment, promoting apoptotic cell death^[1].
6-Methoxydihydrosanguinarine (0.5-2 μM; 24 h) hydrochloride dose-dependently inhibits the Akt/mTOR signaling pathway in A549 and H1299 NSCLC cells after 24 h treatment by reducing Akt and p70S6K phosphorylation and total protein levels^[1].
6-Methoxydihydrosanguinarine (0.5-2 μM; 24 h) hydrochloride dose-dependently blocks the YAP/TAZ oncogenic signaling axis in A549 and H1299 NSCLC cells after 24 h treatment by reducing YAP, TAZ, and survivin expression and increasing LATS1/2 phosphorylation^[1].
6-Methoxydihydrosanguinarine (0.5-2 μM; 24 h) hydrochloride dose-dependently induces apoptosis in A549 and H1299 NSCLC cells after 24 h treatment^[1].
6-Methoxydihydrosanguinarine (0.5-2 μM; 12 h) hydrochloride dose-dependently elevates intracellular ROS levels in A549 and H1299 NSCLC cells after 12 h treatment^[1].
6-Methoxydihydrosanguinarine (0.5-2 μM; 24 h) hydrochloride dose-dependently activates the IRE1/JNK signaling pathway in A549 and H1299 NSCLC cells after 24 h treatment^[1].
6-Methoxydihydrosanguinarine (0.125-8 μM; 24 h) hydrochloride dose-dependently reduces cell viability in HepG2 and Huh7 cells, with IC₅₀ values of 2.83 μM and 3.46 μM after 24 h of treatment^[2].
6-Methoxydihydrosanguinarine hydrochloride (6-MS) (1-2 μM; 12 h) hydrochloride dose-dependently increases intracellular ROS production in HepG2 and Huh7 cells after 12 h of treatment^[2].
6-Methoxydihydrosanguinarine (0.5-2 μM; 24 h) hydrochloride dose-dependently inhibits the EGFR/Akt signaling pathway, as measured by reduced EGFR expression and Akt phosphorylation, in HepG2 and Huh7 cells after 24 h of treatment^[2].
6-Methoxydihydrosanguinarine (0.5-2 μM; 24 h) hydrochloride activates the JNK and p38MAPK pathways in HepG2 and Huh7 cells after 24 h of treatment, with JNK activation being required for 6-MS-induced PARP cleavage (a marker of apoptosis)^[2].
6-Methoxydihydrosanguinarine (0.5-2 μM; 24 h) hydrochloride dose-dependently upregulates DR4 and DR5 expression in HepG2 and Huh7 cells after 24 h of treatment, and DR5 upregulation is required for 6-Methoxydihydrosanguinarine hydrochloride-mediated sensitization to TRAIL-induced apoptosis^[2].
6-Methoxydihydrosanguinarine (0-1.5 μM; 12 h) hydrochloride potently inhibits the viability of HLE and HCCLM3 hepatocellular carcinoma cells with IC₅₀ values of 1.129 μM and 1.308 μM respectively after 12 h, and is less cytotoxic to normal LX-2 hepatic stellate cells^[3].
6-Methoxydihydrosanguinarine (1 μM (HLE), 1.5 μM (HCCLM3); 12 h) hydrochloride induces cell death in hepatocellular carcinoma cells after 12 h of treatment, and this effect is mediated via ferroptosis, as shown by reversal with ferroptosis inhibitors^[3].
6-Methoxydihydrosanguinarine (1 μM (HLE), 1.5 μM (HCCLM3); 6 h) hydrochloride downregulates GPX4 expression at the transcriptional level in hepatocellular carcinoma cells after 6 h of treatment^[3].
6-Methoxydihydrosanguinarine (1-50 μM; 24 h) hydrochloride selectively inhibits human A375 melanoma cell viability over normal NHDF cells, with an IC₅₀ of 2.85 μM after 24 h^[4].
6-Methoxydihydrosanguinarine (0-32 μM; 24 h) hydrochloride potently reduces MCF-7 breast cancer cell viability in a time- and dose-dependent manner, with an IC₅₀ of 4.21 μM after 24 h^[5].
6-Methoxydihydrosanguinarine (2-4 μM; 6-24 h) hydrochloride induces apoptosis in MCF-7 breast cancer cells by upregulating pro-apoptotic proteins and downregulating anti-apoptotic proteins, induces autophagy by upregulating autophagy-related proteins, and inhibits the PI3K/AKT/mTOR pathway by reducing phosphorylation of key pathway proteins^[5].
6-Methoxydihydrosanguinarine hydrochloride downregulates the expression of EFG1, CDC35, RAS1, and TPK2, all of which are critical components of the cAMP pathway. Furthermore, 6-Methoxydihydrosanguinarine hydrochloride changes the membrane permeability of C. albicans and caused reactive oxygen species accumulation, leading to cell death^[6].

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

6-Methoxydihydrosanguinarine (5 mg/kg; i.p.; daily; 14 days) hydrochloride decreases tumor volume and weight in a Caov-3 ovarian cancer mouse xenograft model^[7].

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

399.82

C₂₁H₁₈ClNO₅

CN1C2=C3C(C=C4OCOC4=C3)=CC=C2C5=C(C6=C(OCO6)C=C5)C1OC.Cl

Room temperature in continental US; may vary elsewhere.

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

• [1]. Liu Y, et al. Activity of 6-methoxydihydrosanguinarine from Hylomecon japonica against wild-type and fluconazole-resistant Candida albicans biofilms. J Asian Nat Prod Res. 2025 Jul 28:1-12.  [Content Brief]

  [2]. Zhang H, et al. A novel mechanism of 6-methoxydihydroavicine in suppressing ovarian carcinoma by disrupting mitochondrial homeostasis and triggering ROS/ MAPK mediated apoptosis. Front Pharmacol. 2023 May 5;14:1093650.  [Content Brief]

  [3]. Qi X, et al. 6-Methoxydihydrosanguinarine Suppresses the Proliferation of Non-small Cell Lung Cancer Cells through Elevation of ROS and Activation of IRE1/JNK Signaling. Cell Biochem Biophys. 2025 Dec;83(4):5307-5319.  [Content Brief]

  [4]. Wang LL, et al. 6-Methoxydihydrosanguinarine exhibits cytotoxicity and sensitizes TRAIL-induced apoptosis of hepatocellular carcinoma cells through ROS-mediated upregulation of DR5. Med Oncol. 2023;40(9):266. Published 2023 Aug 11.  [Content Brief]

  [5]. Han L, et al. Bioactive natural alkaloid 6-Methoxydihydrosanguinarine exerts anti-tumor effects in hepatocellular carcinoma cells via ferroptosis. Front Pharmacol. 2025;16:1500461. Published 2025 Apr 24.  [Content Brief]

  [6]. Zuo C, et al. Molecular interactions between fibrinogen and 6-methoxydihydrosanguinarine and their modulation of anticancer activity in melanoma A375 cells. Int J Biol Macromol. 2025;307(Pt 4):142170.  [Content Brief]

  [7]. Zhang L, et al. 6-Methoxydihydrosanguinarine induces apoptosis and autophagy in breast cancer MCF-7 cells by accumulating ROS to suppress the PI3K/AKT/mTOR signaling pathway. Phytother Res. 2023;37(1):124-139.  [Content Brief]