Maackiain
CAS No. : 19908-48-6
(Synonyms: DL-Maackiain)
Price and Availability of
CAS No. : 19908-48-6
| Size | Price | Stock |
|---|---|---|
| 1mg | $37 | In-stock |
| 5mg | $75 | In-stock |
| 10mg | $110 | In-stock |
| 50 mg | Get quote | |
| 100 mg | Get quote | |
| We match the lowest price on market. | ||
We offer a substantial discount on larger orders, please inquire via [email protected]
or Fax: (86)21-58955996
Inquiry for price and availability only. Please place your order via our email or fax.
| Cat. No. : | HY-N0381 |
| M.Wt: | 284.27 |
| Formula: | C16H12O5 |
| Purity: | >98 % |
| Solubility: | DMSO : 250 mg/mL (ultrasonic) |
Introduction of
19908-48-6
:
Maackiain (10-100 ng/mL; pre-incubated for 30 min; co-incubated with LPS for 24 h) inhibits LPS-induced production of proinflammatory cytokines IL-1β, IL-6 and TNF-α in RAW264.7 cells in a dose-dependent manner, suppresses LPS-induced nuclear translocation of NF-κB p65 in RAW264.7 cells, and attenuates oxidative stress by reducing ROS generation, restoring mitochondrial membrane potential, and reversing the levels of GSH, MDA and TEAC[1].
Maackiain (100 ng/mL; pre-incubated for 3 h following pretreatment with AMPK/Nrf2 inhibitors, then co-incubated with LPS for 24 h) exerts antioxidant and anti-inflammatory activities in RAW264.7 cells by activating the AMPK/Nrf2/HO-1 pathway[1].
Maackiain (10-50 μM; 6 h) dose-dependently inhibits Aβ42 (10 μM; 24 h)-induced apoptosis, oxidative stress, inflammatory response, cellular damage and loss of viability in PC12 cells; it also promotes nuclear translocation of Nrf2 in PC12 cells without altering the total expression of Nrf2[2].
Maackiain (5-40 μM; 5 days) dose-dependently inhibits RANKL-induced osteoclast formation in mouse bone marrow macrophages, and at the dose of 40 μM, disrupts the formation of functional F-actin belts in mature mouse osteoclasts[3].
Maackiain (20-40 μM; 5 days) downregulates the expression of key genes associated with osteoclast differentiation and function in RANKL-stimulated mouse bone marrow macrophages[3].
Maackiain (40 μM; 1-5 days) suppresses the expression of osteoclast-specific proteins c-Fos, Integrin β3, MMP9, CTSK and NFATc1 in RANKL-stimulated mouse bone marrow macrophages; meanwhile, it downregulates the protein level of NFATc1 and inhibits its nuclear translocation[3].
Maackiain (40 μM; 1 h) blocks IκB-α degradation and p65 phosphorylation, inhibits RANKL-induced activation of the NF-κB pathway in mouse bone marrow-derived macrophages, and thereby attenuates RANKL-induced calcium oscillations in mouse bone marrow-derived macrophages[3].
Maackiain (50-100 ng/mL; sequential treatment for 1 h after 3 h of LPS pre-treatment and 1 h of incubation with 5 μM nigericin (HY-127019)) enhances 5 μM nigericin-induced caspase-1 activation and mature IL-1β production in LPS-pretreated human monocytic cell line dTHP-1, and exhibits a dose-dependent effect at concentrations of 50 ng/mL and 100 ng/mL[4].
Maackiain (2.5-40 μM; 24 h after LPS incubation) potently inhibits NO production in LPS-stimulated BV2 microglia, with the strongest effect observed at 20 μM, and exhibits a concentration-dependent response at concentrations below 20 μM[5].
Maackiain (10-40 μM; 24 h after LPS incubation) potently inhibits LPS-induced lipid peroxidation in BV2 microglial cells, and the antioxidant activity at the dose of 40 μM is stronger than that of Ferrostatin-1[5].
Maackiain (100 ng/mL; 24 h) inhibits the proliferation of human cervical cancer HeLa and SiHa cells in a concentration-dependent manner, induces autophagy (elevated expression levels of LC3-II and Beclin-1, autophagosome formation) in human cervical cancer HeLa and SiHa cells, and induces cell apoptosis[6].
Maackiain (75 μM; 3 days) induces DNA fragmentation and apoptotic body formation in human promyelocytic leukemia HL-60 cells, and this effect is inhibited by pretreatment with the antioxidant N-acetyl-L-cysteine (5 mM; 2 h pre-incubation)[7].
(-)-maackiain (50-150 μM; 24 h) inhibits the upregulation of IL-4 mRNA in IgE/antigen-induced RBL-2H3 cells, whereas the synthetic (+)-maackiain exerts no significant inhibitory activity[8].
(-)-Maackiain (20, 40 μM; 24 h) inhibits PMA-induced phosphorylation of Tyr311 on PKCδ in HeLa cells[8].
(-)-Maackiain (30 μM; 24 h) inhibits phorbol 12-myristate 13-acetate (PMA)-induced translocation of protein kinase Cδ (PKCδ) to the Golgi apparatus in HeLa cells[8]. In Vivo:Maackiain (2.5-5 mg/kg; i.p.; single dose 12 hours pre-CLP) protects against CLP-induced sepsis in mice via dose-dependent reductions in mortality, organ injury, systemic inflammation, and oxidative stress, with the 5 mg/kg dose reducing 7-day mortality to 40%[1].
Maackiain (25-50 mg/kg; i.g.; daily; 14 days) improves LPS-induced cognitive impairment, increases normal neuron counts, inhibits microglial activation, and reduces cortical pro-inflammatory mediator levels in male C57BL/6 mice, with the 50 mg/kg dose demonstrating superior efficacy in most metrics[5].
Maackiain (5 mg/kg; i.p.; once every 2 days; 6 total injections) reduces cervical tumor weight to ~40% of control levels and inhibits tumor growth by 50% relative to controls without causing significant systemic toxicity in nude mice[6].
Racemic maackiain (5-20 mg/kg; p.o.; daily; 21 days) alleviates TDI-induced allergic rhinitis symptoms and suppresses TDI-induced upregulation of H1R and IL-4 gene expression in Brown Norway rats, with significant effects observed at doses of 5, 10, and 20 mg/kg administered orally daily for 21 days[8].
Maackiain (10-50 μg/mL; immersion; single exposure) demonstrates potent larvicidal activity against Aedes aegypti 4th instar larvae, with an LC50 of 21.95 ± 1.34 μg/mL at 48 hours[9].
Maackiain (DL-Maackiain) is an orally active multi-target inhibitor with anti-tumor activity and neuroprotective effects. Maackiain activates the AMPK, NLRP3 and Nrf2/HO-1 pathways, and inhibits key targets such as NF-κB, mTOR, MAO-B, NFATc1 and PKCδ, thereby precisely regulating processes including apoptosis, autophagy and pyroptosis. Maackiain also effectively inhibits microglial activation, osteoclast formation, and proliferation and invasion of tumor cells, and protects dopaminergic neurons from damage. Maackiain is applicable to the research of various diseases such as Alzheimer's disease, osteoporosis, sepsis and dengue fever[1][2][3][4][5][6][7][8][9]。
IC50 & Target:LD50: 21.95 µg/mL (Aedes aegypti mosquito.xp Parasitol)[1]
In Vitro:Maackiain exhibits no direct bactericidal or bacteriostatic activity against Escherichia coli, Enterobacter cloacae, or Staphylococcus aureus[1].Maackiain (10-100 ng/mL; pre-incubated for 30 min; co-incubated with LPS for 24 h) inhibits LPS-induced production of proinflammatory cytokines IL-1β, IL-6 and TNF-α in RAW264.7 cells in a dose-dependent manner, suppresses LPS-induced nuclear translocation of NF-κB p65 in RAW264.7 cells, and attenuates oxidative stress by reducing ROS generation, restoring mitochondrial membrane potential, and reversing the levels of GSH, MDA and TEAC[1].
Maackiain (100 ng/mL; pre-incubated for 3 h following pretreatment with AMPK/Nrf2 inhibitors, then co-incubated with LPS for 24 h) exerts antioxidant and anti-inflammatory activities in RAW264.7 cells by activating the AMPK/Nrf2/HO-1 pathway[1].
Maackiain (10-50 μM; 6 h) dose-dependently inhibits Aβ42 (10 μM; 24 h)-induced apoptosis, oxidative stress, inflammatory response, cellular damage and loss of viability in PC12 cells; it also promotes nuclear translocation of Nrf2 in PC12 cells without altering the total expression of Nrf2[2].
Maackiain (5-40 μM; 5 days) dose-dependently inhibits RANKL-induced osteoclast formation in mouse bone marrow macrophages, and at the dose of 40 μM, disrupts the formation of functional F-actin belts in mature mouse osteoclasts[3].
Maackiain (20-40 μM; 5 days) downregulates the expression of key genes associated with osteoclast differentiation and function in RANKL-stimulated mouse bone marrow macrophages[3].
Maackiain (40 μM; 1-5 days) suppresses the expression of osteoclast-specific proteins c-Fos, Integrin β3, MMP9, CTSK and NFATc1 in RANKL-stimulated mouse bone marrow macrophages; meanwhile, it downregulates the protein level of NFATc1 and inhibits its nuclear translocation[3].
Maackiain (40 μM; 1 h) blocks IκB-α degradation and p65 phosphorylation, inhibits RANKL-induced activation of the NF-κB pathway in mouse bone marrow-derived macrophages, and thereby attenuates RANKL-induced calcium oscillations in mouse bone marrow-derived macrophages[3].
Maackiain (50-100 ng/mL; sequential treatment for 1 h after 3 h of LPS pre-treatment and 1 h of incubation with 5 μM nigericin (HY-127019)) enhances 5 μM nigericin-induced caspase-1 activation and mature IL-1β production in LPS-pretreated human monocytic cell line dTHP-1, and exhibits a dose-dependent effect at concentrations of 50 ng/mL and 100 ng/mL[4].
Maackiain (2.5-40 μM; 24 h after LPS incubation) potently inhibits NO production in LPS-stimulated BV2 microglia, with the strongest effect observed at 20 μM, and exhibits a concentration-dependent response at concentrations below 20 μM[5].
Maackiain (10-40 μM; 24 h after LPS incubation) potently inhibits LPS-induced lipid peroxidation in BV2 microglial cells, and the antioxidant activity at the dose of 40 μM is stronger than that of Ferrostatin-1[5].
Maackiain (100 ng/mL; 24 h) inhibits the proliferation of human cervical cancer HeLa and SiHa cells in a concentration-dependent manner, induces autophagy (elevated expression levels of LC3-II and Beclin-1, autophagosome formation) in human cervical cancer HeLa and SiHa cells, and induces cell apoptosis[6].
Maackiain (75 μM; 3 days) induces DNA fragmentation and apoptotic body formation in human promyelocytic leukemia HL-60 cells, and this effect is inhibited by pretreatment with the antioxidant N-acetyl-L-cysteine (5 mM; 2 h pre-incubation)[7].
(-)-maackiain (50-150 μM; 24 h) inhibits the upregulation of IL-4 mRNA in IgE/antigen-induced RBL-2H3 cells, whereas the synthetic (+)-maackiain exerts no significant inhibitory activity[8].
(-)-Maackiain (20, 40 μM; 24 h) inhibits PMA-induced phosphorylation of Tyr311 on PKCδ in HeLa cells[8].
(-)-Maackiain (30 μM; 24 h) inhibits phorbol 12-myristate 13-acetate (PMA)-induced translocation of protein kinase Cδ (PKCδ) to the Golgi apparatus in HeLa cells[8]. In Vivo:Maackiain (2.5-5 mg/kg; i.p.; single dose 12 hours pre-CLP) protects against CLP-induced sepsis in mice via dose-dependent reductions in mortality, organ injury, systemic inflammation, and oxidative stress, with the 5 mg/kg dose reducing 7-day mortality to 40%[1].
Maackiain (25-50 mg/kg; i.g.; daily; 14 days) improves LPS-induced cognitive impairment, increases normal neuron counts, inhibits microglial activation, and reduces cortical pro-inflammatory mediator levels in male C57BL/6 mice, with the 50 mg/kg dose demonstrating superior efficacy in most metrics[5].
Maackiain (5 mg/kg; i.p.; once every 2 days; 6 total injections) reduces cervical tumor weight to ~40% of control levels and inhibits tumor growth by 50% relative to controls without causing significant systemic toxicity in nude mice[6].
Racemic maackiain (5-20 mg/kg; p.o.; daily; 21 days) alleviates TDI-induced allergic rhinitis symptoms and suppresses TDI-induced upregulation of H1R and IL-4 gene expression in Brown Norway rats, with significant effects observed at doses of 5, 10, and 20 mg/kg administered orally daily for 21 days[8].
Maackiain (10-50 μg/mL; immersion; single exposure) demonstrates potent larvicidal activity against Aedes aegypti 4th instar larvae, with an LC50 of 21.95 ± 1.34 μg/mL at 48 hours[9].
Lorem ipsum dolor sit amet, consectetur adipisicing elit. Autem earum hic iste maiores, nam neque rem suscipit. Adipisci consequatur error exercitationem fugit ipsam optio qui, quibusdam repellendus sed vero! Debitis.
Inquiry Information- Product Name:
- Maackiain
- Cat. No.:
- HY-N0381
- Quantity:
Your information is safe with us.