ACT001 hydrochloride (Synonyms: Dimethylaminomicheliolide hydrochloride; DMAMCL hydrochloride) |
カタログ番号GC78965
One-Click Copy Product Info
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ACT001 (Dimethylaminomicheliolide; DMAMCL) hydrochloride is an orally active, blood-brain barrier-permeable anti-inflammatory and anti-tumor agent.
Products are for research use only. Not for human use. We do not sell to patients.
Cas No.: 1403357-80-1
Sample solution is provided at 25 µL, 10mM.
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ACT001 (Dimethylaminomicheliolide; DMAMCL) hydrochloride is an orally active, blood-brain barrier-permeable anti-inflammatory and anti-tumor agent. ACT001 hydrochloride exerts microglia-mediated neuroanti-inflammatory effects by inhibiting the AKT/NF-κB/NLRP3 axis and suppressing apoptosis ( apoptosis ). ACT001 hydrochloride inhibits tumor proliferation by upregulating NKTR and inhibiting AKT. ACT001 hydrochloride alleviates metabolic-associated fatty liver disease by regulating gut microbiota and inhibiting ileal FXR. ACT001 hydrochloride inhibits pyroptosis ( pyroptosis ) and pro-inflammatory cytokine release by activating PPAR-γ and inhibiting NF-κB/NLRP3 [1] [2] [3] [4].
In Vivo, ACT001 hydrochloride ameliorates ionizing radiation-induced acute lung injury in Sprague-Dawley rats by inhibiting NLRP3 inflammasome activation, pyroptosis and inflammatory responses[1]. ACT001 (200 mg/kg; p.o.; once daily; for 12 consecutive days) hydrochloride significantly inhibits the growth of non-small cell lung cancer xenografts in BALB/c nude mice, upregulates NKTR expression, downregulates Ki67 expression, and causes no hepatotoxicity or nephrotoxicity[2]. ACT001 (100 mg/kg; p.o.; once daily; for 7 consecutive days) hydrochloride reduces the lesion volume induced by traumatic brain injury (TBI) by 5.36% in male C57BL/6 mice on day 7 post-injury. It improves blood-brain barrier (BBB) integrity and promotes neurobehavioral recovery by inhibiting microglial activation and neuronal apoptosis[3]. The neuroprotective efficacy of ACT001 (100 mg/kg; p.o.; once daily; for 7 consecutive days) hydrochloride is significantly reduced in male C57BL/6 mice with traumatic brain injury (TBI) whose microglia are depleted by PLX5622[3]. ACT001 (200 mg/kg/d; oral administration; daily dosing; for 20 consecutive weeks) hydrochloride alleviates metabolic dysfunction-associated steatotic liver disease (MASLD) induced by high-fat diet (HFD) in female C57BL/6J mice, significantly reduces hepatic aspartate transaminase (AST) and triglyceride (TG) levels, restores intestinal barrier function, modulates gut microbiota, and regulates the bile acid-FXR-FGF15 axis[4]. ACT001 (200 mg/kg/d; oral administration; daily dosing; for 6 consecutive weeks) hydrochloride alleviates MCD-induced MASLD in female C57BL/6J mice, significantly reduces the levels of intestinal inflammatory markers, modulates the gut microbiota, and regulates the bile acid-FXR-FGF15 axis[4].
In Vitro, ACT001 (10-40 µM; 28 h) dose-dependently reduces the secretion levels of pro-inflammatory cytokines (TNF-α, IL-6, IL-1β, IL-18) and increases the secretion level of the anti-inflammatory cytokine IL-10 in LPS -stimulated NR8383 rat alveolar macrophages[1]. ACT001 (10-40 µM; 28 h) dose-dependently reduces the mRNA expression of pro-inflammatory cytokines (TNF-α, IL-6, IL-1β, IL-18) and increases the mRNA expression of the anti-inflammatory cytokine IL-10 in LPS-stimulated NR8383 rat alveolar macrophages[1]. ACT001 (10-40 µM; 28 h) dose-dependently reduces the pyroptosis level of LPS-stimulated NR8383 rat alveolar macrophages, as determined by caspase-1 activity assay and PI staining[1]. ACT001 (10-40 µM; 28 h) dose-dependently reduces the protein expression of NLRP3 inflammasome components (NLRP3, ASC) and pyroptosis mediators (caspase-1 p20, GSDMD-N) in LPS-stimulated NR8383 rat alveolar macrophages[1]. ACT001 (10-40 µM; 28 h) dose-dependently upregulates the expression of PPAR-γ in LPS-stimulated NR8383 rat alveolar macrophages and inhibits the activation of the NF-κB pathway (reducing the phosphorylation levels of IκB-α and NF-κB p65), while PPAR-γ inhibitors reverse these anti-inflammatory/anti-pyroptotic effects[1]. ACT001 (0.0625-800 μM; 72 h) potently inhibits the viability of non-small cell lung cancer (NSCLC) cell lines, with the strongest activity against H1703 cells (IC50 = 9.21 μM) and H1975 cells (IC50 = 14.42 μM) after 72 hours of treatment[2]. ACT001 (10-20 μM; 10-14 days) inhibits the clonal proliferation of H1703 and H1975 non-small cell lung cancer (NSCLC) cells in a dose-dependent manner[2]. ACT001 (10-20 μM) alters gene expression in H1703 non-small cell lung cancer (NSCLC) cells, among which the cell cycle pathway is most significantly affected, and NKTR is one of the most significantly upregulated genes[2]. ACT001 (10-20 μM) induces G1/S cell cycle arrest in H1703 and H1975 non-small cell lung cancer (NSCLC) cells[2]. ACT001 (10-20 μM) downregulates the expression of cyclinD1 and CDK6 in H1703 and H1975 non-small cell lung cancer (NSCLC) cells[2]. ACT001 (10-20 μM) dose-dependently inhibits AKT phosphorylation in H1703 and H1975 non-small cell lung cancer (NSCLC) cells without altering the expression of total AKT[2]. ACT001 (10-20 μM) upregulates the mRNA and protein expression of NKTR in H1703 and H1975 non-small cell lung cancer (NSCLC) cells in a dose-dependent manner[2]. ACT001 (20 μM) upregulates the mRNA and protein expression of NKTR, even in NKTR-knockdown H1703 and H1975 non-small cell lung cancer (NSCLC) cells[2]. ACT001 (1-10 μM; 12-48 h) exhibits no cytotoxicity against mouse microglial BV2 cells at concentrations up to 10 μM and incubation durations of 12-48 h[3]. ACT001 (1-10 μM; 24-48 h) dose-dependently inhibits LPS-induced pro-inflammatory activation of mouse microglial BV2 cells, reduces amoeboid morphological changes and the expression of pro-inflammatory cytokines, and increases the expression of anti-inflammatory cytokines[3]. ACT001 (1-10 μM; 24-48 h) dose-dependently inhibits LPS-induced activation of primary mouse microglia, reduces NO production and the number of CD68+ activated cells, without affecting cell viability[3]. ACT001 (1-10 μM; 24-48 h) dose-dependently inhibits LPS-induced activation of primary rat microglia, reduces NO production and the number of CD68+ activated cells, without affecting cell viability[3]. ACT001 (1-10 μM; 24-48 h) dose-dependently reduces neuronal apoptosis of mouse hippocampal HT22 cells induced by LPS-activated mouse microglial BV2 cells in a Transwell co-culture model, accompanied by decreased NO production[3]. ACT001 (1-2 μM; 24 h) dose-dependently alleviates the inhibitory effect of LPS-activated mouse microglial BV2 cells on angiogenesis of mouse brain endothelial bEnd.3 cells, reduces VEGF levels, and restores the expression of tight junction proteins[3]. ACT001 (1-10 μM; 24 h) inhibits the AKT/NFκB/NLRP3 neuroinflammatory pathway in rat primary microglia and mouse microglial BV2 cells by directly binding to AKT, reducing AKT phosphorylation levels, suppressing NFκB nuclear translocation, and inhibiting NLRP3 inflammasome activation[3].
References:
[1]. Fu Q, et al. ACT001 alleviates inflammation and pyroptosis through the PPAR-γ/NF-κB signaling pathway in LPS-induced alveolar macrophages. Genes & genomics. 2024 Mar;46(3):323-332.
[2]. Zhao M, et al. ACT001 inhibits the proliferation of non-small cell lung cancer cells by upregulating NKTR expression. Thoracic cancer. 2022 Jun;13(12):1772-1782.
[3]. Cai L, et al. ACT001 attenuates microglia-mediated neuroinflammation after traumatic brain injury via inhibiting AKT/NFκB/NLRP3 pathway. Cell communication and signaling: CCS. 2022 Apr 23;20(1):56.
[4]. Niu B, et al. ACT001 alleviates MASLD through gut microbiota-bile acid-FXR axis in mice. Annals of medicine. 2025 Dec;57(1):2580773.
In Vivo, ACT001 hydrochloride ameliorates ionizing radiation-induced acute lung injury in Sprague-Dawley rats by inhibiting NLRP3 inflammasome activation, pyroptosis and inflammatory responses[1]. ACT001 (200 mg/kg; p.o.; once daily; for 12 consecutive days) hydrochloride significantly inhibits the growth of non-small cell lung cancer xenografts in BALB/c nude mice, upregulates NKTR expression, downregulates Ki67 expression, and causes no hepatotoxicity or nephrotoxicity[2]. ACT001 (100 mg/kg; p.o.; once daily; for 7 consecutive days) hydrochloride reduces the lesion volume induced by traumatic brain injury (TBI) by 5.36% in male C57BL/6 mice on day 7 post-injury. It improves blood-brain barrier (BBB) integrity and promotes neurobehavioral recovery by inhibiting microglial activation and neuronal apoptosis[3]. The neuroprotective efficacy of ACT001 (100 mg/kg; p.o.; once daily; for 7 consecutive days) hydrochloride is significantly reduced in male C57BL/6 mice with traumatic brain injury (TBI) whose microglia are depleted by PLX5622[3]. ACT001 (200 mg/kg/d; oral administration; daily dosing; for 20 consecutive weeks) hydrochloride alleviates metabolic dysfunction-associated steatotic liver disease (MASLD) induced by high-fat diet (HFD) in female C57BL/6J mice, significantly reduces hepatic aspartate transaminase (AST) and triglyceride (TG) levels, restores intestinal barrier function, modulates gut microbiota, and regulates the bile acid-FXR-FGF15 axis[4]. ACT001 (200 mg/kg/d; oral administration; daily dosing; for 6 consecutive weeks) hydrochloride alleviates MCD-induced MASLD in female C57BL/6J mice, significantly reduces the levels of intestinal inflammatory markers, modulates the gut microbiota, and regulates the bile acid-FXR-FGF15 axis[4].
In Vitro, ACT001 (10-40 µM; 28 h) dose-dependently reduces the secretion levels of pro-inflammatory cytokines (TNF-α, IL-6, IL-1β, IL-18) and increases the secretion level of the anti-inflammatory cytokine IL-10 in LPS -stimulated NR8383 rat alveolar macrophages[1]. ACT001 (10-40 µM; 28 h) dose-dependently reduces the mRNA expression of pro-inflammatory cytokines (TNF-α, IL-6, IL-1β, IL-18) and increases the mRNA expression of the anti-inflammatory cytokine IL-10 in LPS-stimulated NR8383 rat alveolar macrophages[1]. ACT001 (10-40 µM; 28 h) dose-dependently reduces the pyroptosis level of LPS-stimulated NR8383 rat alveolar macrophages, as determined by caspase-1 activity assay and PI staining[1]. ACT001 (10-40 µM; 28 h) dose-dependently reduces the protein expression of NLRP3 inflammasome components (NLRP3, ASC) and pyroptosis mediators (caspase-1 p20, GSDMD-N) in LPS-stimulated NR8383 rat alveolar macrophages[1]. ACT001 (10-40 µM; 28 h) dose-dependently upregulates the expression of PPAR-γ in LPS-stimulated NR8383 rat alveolar macrophages and inhibits the activation of the NF-κB pathway (reducing the phosphorylation levels of IκB-α and NF-κB p65), while PPAR-γ inhibitors reverse these anti-inflammatory/anti-pyroptotic effects[1]. ACT001 (0.0625-800 μM; 72 h) potently inhibits the viability of non-small cell lung cancer (NSCLC) cell lines, with the strongest activity against H1703 cells (IC50 = 9.21 μM) and H1975 cells (IC50 = 14.42 μM) after 72 hours of treatment[2]. ACT001 (10-20 μM; 10-14 days) inhibits the clonal proliferation of H1703 and H1975 non-small cell lung cancer (NSCLC) cells in a dose-dependent manner[2]. ACT001 (10-20 μM) alters gene expression in H1703 non-small cell lung cancer (NSCLC) cells, among which the cell cycle pathway is most significantly affected, and NKTR is one of the most significantly upregulated genes[2]. ACT001 (10-20 μM) induces G1/S cell cycle arrest in H1703 and H1975 non-small cell lung cancer (NSCLC) cells[2]. ACT001 (10-20 μM) downregulates the expression of cyclinD1 and CDK6 in H1703 and H1975 non-small cell lung cancer (NSCLC) cells[2]. ACT001 (10-20 μM) dose-dependently inhibits AKT phosphorylation in H1703 and H1975 non-small cell lung cancer (NSCLC) cells without altering the expression of total AKT[2]. ACT001 (10-20 μM) upregulates the mRNA and protein expression of NKTR in H1703 and H1975 non-small cell lung cancer (NSCLC) cells in a dose-dependent manner[2]. ACT001 (20 μM) upregulates the mRNA and protein expression of NKTR, even in NKTR-knockdown H1703 and H1975 non-small cell lung cancer (NSCLC) cells[2]. ACT001 (1-10 μM; 12-48 h) exhibits no cytotoxicity against mouse microglial BV2 cells at concentrations up to 10 μM and incubation durations of 12-48 h[3]. ACT001 (1-10 μM; 24-48 h) dose-dependently inhibits LPS-induced pro-inflammatory activation of mouse microglial BV2 cells, reduces amoeboid morphological changes and the expression of pro-inflammatory cytokines, and increases the expression of anti-inflammatory cytokines[3]. ACT001 (1-10 μM; 24-48 h) dose-dependently inhibits LPS-induced activation of primary mouse microglia, reduces NO production and the number of CD68+ activated cells, without affecting cell viability[3]. ACT001 (1-10 μM; 24-48 h) dose-dependently inhibits LPS-induced activation of primary rat microglia, reduces NO production and the number of CD68+ activated cells, without affecting cell viability[3]. ACT001 (1-10 μM; 24-48 h) dose-dependently reduces neuronal apoptosis of mouse hippocampal HT22 cells induced by LPS-activated mouse microglial BV2 cells in a Transwell co-culture model, accompanied by decreased NO production[3]. ACT001 (1-2 μM; 24 h) dose-dependently alleviates the inhibitory effect of LPS-activated mouse microglial BV2 cells on angiogenesis of mouse brain endothelial bEnd.3 cells, reduces VEGF levels, and restores the expression of tight junction proteins[3]. ACT001 (1-10 μM; 24 h) inhibits the AKT/NFκB/NLRP3 neuroinflammatory pathway in rat primary microglia and mouse microglial BV2 cells by directly binding to AKT, reducing AKT phosphorylation levels, suppressing NFκB nuclear translocation, and inhibiting NLRP3 inflammasome activation[3].
References:
[1]. Fu Q, et al. ACT001 alleviates inflammation and pyroptosis through the PPAR-γ/NF-κB signaling pathway in LPS-induced alveolar macrophages. Genes & genomics. 2024 Mar;46(3):323-332.
[2]. Zhao M, et al. ACT001 inhibits the proliferation of non-small cell lung cancer cells by upregulating NKTR expression. Thoracic cancer. 2022 Jun;13(12):1772-1782.
[3]. Cai L, et al. ACT001 attenuates microglia-mediated neuroinflammation after traumatic brain injury via inhibiting AKT/NFκB/NLRP3 pathway. Cell communication and signaling: CCS. 2022 Apr 23;20(1):56.
[4]. Niu B, et al. ACT001 alleviates MASLD through gut microbiota-bile acid-FXR axis in mice. Annals of medicine. 2025 Dec;57(1):2580773.
| Cas No. | 1403357-80-1 | SDF | |
| 同義語 | Dimethylaminomicheliolide hydrochloride; DMAMCL hydrochloride | ||
| Formula | C17H28ClNO3 | M.Wt | 329.86 |
| 溶解度 | Storage | Store at -20°C | |
| Shipping Condition | Evaluation sample solution: shipped with blue ice. All other sizes available: with RT, or with Blue Ice upon request. | ||
| Prepare stock solution | |||
|
1 mg | 5 mg | 10 mg |
| 1 mM | 3.0316 mL | 15.1579 mL | 30.3159 mL |
| 5 mM | 606.3 μL | 3.0316 mL | 6.0632 mL |
| 10 mM | 303.2 μL | 1.5158 mL | 3.0316 mL |
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- Purity: >98.00% Appearance: A solid
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Review for ACT001 hydrochloride
Average Rating: 5 (Based on Reviews and 30 reference(s) in Google Scholar.)