Matairesinol 

Matairesinol is an orally active bioactive compound with anti-inflammatory, antioxidant and anticancer activities. Matairesinol inhibits the phosphorylation of MAPK, JNK and NF-κB, downregulates RANKL-induced NFATc1 expression and activity, and suppresses the activation of the PI3K/AKT/FOXO1 pathway. Matairesinol can be used in research related to sepsis-mediated brain injury, osteoporosis, heart failure, atopic dermatitis and cancer^{[1][2][3][4][5]}.

Matairesinol (1-80 μM; 48 h) exhibits minimal toxicity to NSC-34 and HT22 neuronal cells at concentrations up to 40 μM, with significant cytotoxicity only at 80 μM after 48 h of treatment^[1].
Matairesinol (5-20 μM; 48 h) reverses the anti-proliferative and pro-apoptotic effects of LPS on NSC-34 and HT22 neuronal cells, with effects detectable at 24, 48, and 72 h post-treatment^[1].
Matairesinol (5-20 μM; 48 h) attenuates LPS-mediated oxidative stress and inflammation in BV2 microglia, while modulating the expression of Nrf2/HO-1 and inhibiting MAPK/JNK/NF-κB pathway activation^[1].
Matairesinol (0.3-30 μM; 4 days) dose-dependently inhibits RANKL-induced differentiation of mouse bone marrow-derived macrophages into osteoclasts, with significant inhibition observed at concentrations ≥10 μM for osteoclast formation and ≥1 μM for TRAP activity^[2].
Matairesinol (0.3-30 μM; 3 days) does not reduce the viability of mouse bone marrow-derived macrophages^[2].
Matairesinol (10 μM; 1-3 days) suppresses RANKL-induced expression of NFATc1 and downstream osteoclastogenesis-associated genes (TRAP, OSCAR, v-ATPasev0d2) in mouse bone marrow-derived macrophages over 1-3 days of treatment^[2].
Matairesinol (10 μM; 4 days, following 8 h retroviral infection) has its inhibitory effect on RANKL-induced osteoclast differentiation reversed by ectopic overexpression of constitutively active NFATc1 in mouse bone marrow-derived macrophages, confirming NFATc1 as a key mediator of its anti-osteoclastogenic activity^[2].
Matairesinol (10 μM; 1 h pre-incubation, followed by RANKL stimulation for 5, 15, 30 min) suppresses RANKL-induced activation of p38 and ERK (but not JNK) MAPK signaling pathways in mouse bone marrow-derived macrophages^[2].
Matairesinol (0-100 μM) at 50 μM maintains viability in Ang II-stimulated NRVMs, while 100 μM reduces viability under basal conditions^[3].
Matairesinol (50 μM) attenuates Ang II-induced hypertrophy in NRVMs by reducing cell size and suppressing hypertrophy-related gene expression^[3].
Matairesinol (50 μM) inhibits Ang II-induced activation of NRCFs by reducing fibrotic marker expression and suppressing the TGF-β/Smad3 pathway^[3].
Matairesinol (50 μM) ameliorates oxidative stress in Ang II-stimulated NRVMs by reducing ROS levels^[3].
Matairesinol (10-500 μM; 72 h) inhibits proliferation of HUVECs (IC₅₀ 75 μM) more potently than HeLa cells (IC₅₀ 200 μM)^[5].
Matairesinol (10-100 μM; 48 h, 72 h) does not induce cytotoxicity in HUVECs at concentrations up to 50 μM when treated for 72 h, or at 100 μM when treated for 48 h^[5].
Matairesinol (10-20 μM; 3-16 h) dose-dependently inhibits VEGF-induced capillary tube formation in serum-starved HUVECs^[5].
Matairesinol (20-80 μM) dose-dependently reduces PCNA protein expression in PANC-1 and MIA PaCa-2 pancreatic cancer cells, with 80 μM causing a 30% and 33% reduction in the respective cell lines^[6].
Matairesinol (80 μM; 3 days) inhibits 3D spheroid formation in PANC-1 and MIA PaCa-2 pancreatic cancer cells, reducing spheroid area by 78% and 61% in the respective cell lines^[6].
Matairesinol (20-80 μM; 48 h) dose-dependently induces late apoptosis in PANC-1 and MIA PaCa-2 pancreatic cancer cells, with 80 μM increasing late apoptosis by 196% and 261% in the respective cell lines over 48 h^[6].
Matairesinol (20-80 μM; 1 h) dose-dependently increases intracellular ROS production in PANC-1 and MIA PaCa-2 pancreatic cancer cells, with 80 μM increasing ROS by 447% and 548% in the respective cell lines after 1 h^[6].
Matairesinol (20-80 μM; 48 h) dose-dependently increases cytosolic calcium levels in PANC-1 and MIA PaCa-2 pancreatic cancer cells, with 80 μM increasing levels by 280% and 551% in the respective cell lines over 48 h^[6].

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

Matairesinol (5-20 mg/kg; p.o.; single dose) concentration-dependently reduces sepsis-mediated brain injury in CLP-induced rats by exerting anti-inflammatory, antioxidant, and neuroprotective effects via up-regulating AMPK and inhibiting MAPK and NF-κB pathways^[1].
Matairesinol (100 mg·kg⁻¹·d⁻¹; intraperitoneal injection; daily; 3 weeks) improves cardiac function, reduces cardiac hypertrophy and remodeling, inhibits cardiomyocyte apoptosis, and mitigates oxidative stress in TAC-induced mice by upregulating Prdx1 and inhibiting the PI3K/AKT/FOXO1 pathway, with these effects blunted by Prdx1 knockdown^[3].
Matairesinol (topical; daily; 11 days) effectively suppresses DfE-induced atopic dermatitis in NC/Nga mice by reducing ear swelling, serum IgE levels, inflammatory cell infiltration, mast cell numbers, and normalizing IL-4 and IFN-γ mRNA expression^[4].

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

358.39

C₂₀H₂₂O₆

580-72-3

Solid

White to yellow

O=C1OC[C@H](CC2=CC=C(O)C(OC)=C2)[C@H]1CC3=CC=C(O)C(OC)=C3

Room temperature in continental US; may vary elsewhere.

4°C, protect from light

*In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)

* Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (protect from light). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

• [1]. Wu Q, et al. Matairesinol exerts anti-inflammatory and antioxidant effects in sepsis-mediated brain injury by repressing the MAPK and NF-κB pathways through up-regulating AMPK. Aging (Albany NY). 2021;13(20):23780-23795.  [Content Brief]

  [2]. Choi SW, et al. Anti-osteoclastogenic activity of matairesinol via suppression of p38/ERK-NFATc1 signaling axis. BMC Complement Altern Med. 2014;14:35. Published 2014 Jan 21.  [Content Brief]

  [3]. Zhang T, et al. Matairesinol blunts adverse cardiac remodeling and heart failure induced by pressure overload by regulating Prdx1 and PI3K/AKT/FOXO1 signaling. Phytomedicine. 2024;135:156054.  [Content Brief]

  [4]. Sung YY, et al. Forsythia suspensa fruit extracts and the constituent matairesinol confer anti-allergic effects in an allergic dermatitis mouse model. J Ethnopharmacol. 2016;187:49-56.  [Content Brief]

  [5]. Lee B, et al. Matairesinol inhibits angiogenesis via suppression of mitochondrial reactive oxygen species. Biochem Biophys Res Commun. 2012;421(1):76-80.  [Content Brief]

  [6]. Lee W, et al. Matairesinol Induces Mitochondrial Dysfunction and Exerts Synergistic Anticancer Effects with 5-Fluorouracil in Pancreatic Cancer Cells. Mar Drugs. 2022;20(8):473. Published 2022 Jul 25.  [Content Brief]