Mahanimbine
(Synonyms: 马汉九里香碱) 目录号 : GC47591
A carbazole alkaloid with diverse biological activities
Cas No.:21104-28-9
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Mahanimbine is a carbazole alkaloid that has been found in M. koenigii and has diverse biological activities.1,2,3 It is active against S. aureus and S. pyogenes (MIC100 = 50 µg/ml for both), as well as A. aegypti fourth instar larvae when used at a concentration of 100 µg/ml.1 Mahanimbine induces cell cycle arrest at the G0/G1 phase and apoptosis in Capan-2 and SW1190 cancer cells when used at a concentration of 7 µM, as well as inhibits proliferation in Capan-2, SW1190, BxPC-3, CFPAC-1, and HPAF-II cancer cells (IC50s = 3.5, 3.5, 16, 64, and 32 µM, respectively).2 It decreases body weight gain without affecting food intake and reduces increases in plasma total cholesterol and triglyceride levels in a rat model of high-fat diet-induced obesity when administered orally at a dose of 30 mg/kg.3
1.Ramsewak, R.S., Nair, M.G., Strasburg, G.M., et al.Biologically active carbazole alkaloids from Murraya koenigiiJ. Agric. Food Chem.47(2)444-447(1999) 2.Pei, C., He, Q., Liang, S., et al.Mahanimbine exerts anticancer effects on human pancreatic cancer cells by triggering cell cycle arrest, apoptosis, and modulation of AKT/mammalian target of rapamycin (mTOR) and signal transducer and activator of transcription 3 (STAT3) signalling pathwaysMed. Sci. Monit.246975-6983(2018) 3.Birari, R., Javia, V., and Bhutani, K.K.Antiobesity and lipid lowering effects of Murraya koenigii (L.) spreng leaves extracts and mahanimbine on high fat diet induced obese ratsFitoterapia81(8)1129-1133(2010)
| Cas No. | 21104-28-9 | SDF | |
| 别名 | 马汉九里香碱 | ||
| Canonical SMILES | C/C(C)=C/CC[C@]1(C)OC2=C(C(NC3=C4C=CC=C3)=C4C=C2C)C=C1 | ||
| 分子式 | C23H25NO | 分子量 | 331.5 |
| 溶解度 | DMSO: 10 mM | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 3.0166 mL | 15.083 mL | 30.1659 mL |
| 5 mM | 0.6033 mL | 3.0166 mL | 6.0332 mL |
| 10 mM | 0.3017 mL | 1.5083 mL | 3.0166 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Mahanimbine isolated from Murraya koenigii inhibits P-glycoprotein involved in lung cancer chemoresistance
Bioorg Chem 2022 Dec;129:106170.PMID:36174443DOI:10.1016/j.bioorg.2022.106170.
P-glycoprotein (P-gp), a transmembrane glycoprotein, is mainly involved in lung cancer multidrug resistance. Several P-gp inhibitors have been developed to enhance the efficacy of chemotherapeutics and overcome drug resistance. However, most of them failed in the clinical stages due to undesirable side effects. Therefore, there is a requirement to develop P-gp inhibitors from natural sources. Dietary spice bioactives have been well-known for their anticancer activities. However, their role in modulating the P-gp activity has not been well investigated. Therefore, we have screened for the potential bioactives from various spice plants with P-gp modulatory activity using computational molecular docking analysis. The computational analysis revealed several key bioactives from curry leaves, specifically Mahanimbine, exhibited a strong binding affinity with P-gp. Unfortunately, Mahanimbine is available with few commercial sources at very high prices. Therefore, we prepared a curry leaves extract and isolated Mahanimbine by a novel, yet simple, extraction method that requires less time and causes minimum environmental hazards. After purification, structure, and mass were confirmed for the isolated compound by IR spectrum and LC-MS/MS analysis, respectively. In the mechanistic study, hydrolysis of ATP and substrate efflux by P-gp are coupled. Hence, ATP binding at the ATPase-binding site is one of the fundamental steps for the P-gp efflux cycle. We found that Mahanimbine demonstrated to stimulate P-gp ATPase activity. Concurrently, it enhanced the intracellular accumulation of P-gp substrates Rhodamine 123 and Hoechst stain, which indicates that Mahanimbine modulates the function of P-gp. In addition, we have analyzed the complementary effect of Mahanimbine with the chemotherapeutic drug gefitinib. We found that Mahanimbine synergistically enhanced gefitinib efficiency by increasing its intracellular accumulation in lung cancer cells. Overall, Mahanimbine has been shown to be a potent P-gp modulator. Therefore, Mahanimbine can be further developed as a potential candidate to overcome chemoresistance in lung cancer.
Mahanimbine Improved Aging-Related Memory Deficits in Mice through Enhanced Cholinergic Transmission and Suppressed Oxidative Stress, Amyloid Levels, and Neuroinflammation
Brain Sci 2021 Dec 23;12(1):12.PMID:35053756DOI:10.3390/brainsci12010012.
Murraya koenigii leaves contain Mahanimbine, a carbazole alkaloid, reported with improving cholinergic neuronal transmission and reducing neuroinflammation in the CNS. The current research investigated the effects of Mahanimbine on age-related memory deficits, oxidative stress, cholinergic dysfunction, amyloid formation, and neuroinflammation in aged mice (16 months old). Mahanimbine was administered (1 and 2 mg/kg, p.o.) daily to groups of aged mice for 30 days. The Morris water maze (MWM) task was performed to study spatial learning (escape latency (EL) and swimming distance (SD)) and memory (probe test). The levels of malondialdehyde (MDA), glutathione (GSH), acetylcholine (ACh), acetylcholinesterase (AChE), β-amyloid (Aβ1-40 and Aβ1-42), β-secretase (BACE-1), as well as neuroinflammation markers (total cyclooxygenase (COX) and COX-2 expression), were measured from the isolated brain. Mahanimbine reduced the EL time and SD in the MWM test. From the probe trial, the mahanimbine-treated group spent more time in the targeted quadrant related to the age-matched control, which indicated the enhancement of memory retention. From the biochemical tests, the treatment decreased MDA, AChE, Aβ1-40, and Aβ1-42, BACE-1, total COX activity, and COX-2 expression. It also raised the brain GSH and ACh levels in aged mice compared to age-matched control. These results have supported the reversal of memory dysfunctions by Mahanimbine in aged mice and hypothesized that it could be a potential target to treat age-related neurodegenerative disease.
Mahanimbine Exerts Anticancer Effects on Human Pancreatic Cancer Cells by Triggering Cell Cycle Arrest, Apoptosis, and Modulation of AKT/Mammalian Target of Rapamycin (mTOR) and Signal Transducer and Activator of Transcription 3 (STAT3) Signalling Pathways
Med Sci Monit 2018 Oct 1;24:6975-6983.PMID:30273298DOI:10.12659/MSM.911013.
BACKGROUND Pancreatic cancer causes tremendous mortality across the globe mainly due to late diagnosis and unavailability of efficient chemotheruptic agents. In the current study the anticancer potential of a plant derived alkaloid, Mahanimbine, was examined against a panel of pancreatic cancer cells. MATERIAL AND METHODS The cell proliferation was determined by MTT assay. Annexin V/PI and DAPI staining were performed to detect apoptosis. Cell cycle distribution was investigated by flow cytometery. Cell migration was detected by wound healing assay and protein expression was checked by western blotting. RESULTS The results revealed that Mahanimbine could inhibit the proliferation of the all the pancreatic cancer cells with lower cytoxicity against the normal cells. The IC50 ranged from 3.5 to 64 µM against the pancreatic cancer cell lines. The lowest IC50 of 3.5 µM was observed tor the Capan-2 and SW119 pancreatic cancer cell lines. The anticancer activity of Mahanimbine against the Capan-2 and SW119 cells was found to be due to G0/G1 cell cycle arrest and induction of apoptosis. Mahanimbine prompted apoptosis was also associated with decline in Bcl-2 and enhancement of the Bax expression. Further, it was observed that Mahanimbine could inhibit the AKT/mTOR and STAT3 signalling pathways in the Capan-2 and SW119 pancreatic cancer cells. The effects of the Mahanimbine were also examined on the migration of the Capan-2 and SW119 pancreatic cancer cells. It was found that Mahanimbine could inhibit the motility and migration of both the pancreatic cancer cell lines. CONCLUSIONS We found that Mahanimbine inhibits the proliferation of pancreatic cancer cells and as such Mahanimbine may prove beneficial in the management of pancreatic cancer.
Anticancer effects of Mahanimbine alkaloid on the human bladder cancer cells are due to the induction of G0/G1 cell cycle arrest, apoptosis and autophagy
J BUON 2020 Mar-Apr;25(2):1166-1171.PMID:32521922doi
Purpose: The main purpose of the current research work was to investigate the anticancer effects of Mahanimbine alkaloid in human bladder cancer cells along with examining its effects on cellular apoptosis, cell cycle phase distribution, and cell autophagy. Methods: Cell viability was examined by WST-1 cell viability assay. Mahanimbine-induced apoptosis was examined by fluorescent microscopy using acridine orange (AO)/ethidium bromide (EB) staining as well as using flow cytometry in combination with annexin-v/propidium iodide (PI) staining. Further, western blot assay was used to study the effects of Mahanimbine on apoptosis-related protein expressions including Bax and Bcl-2. Autophagy induction was evaluated by transmission electron microscopy (TEM) and western blot. Flow cytometry was used to study the effects on cell cycle. Results: The results showed that Mahanimbine decreased the viability of the human bladder cancer cells and exhibited an IC50 of 32.5 µM. The test molecule also caused remarkable changes in the morphology of human bladder cancer cells and inhibited their colony forming potential. The AO/EB staining assay showed that Mahanimbine inhibits the viability of cancer cells via induction of apoptotic cell death which was associated with increase in Bax and decrease in Bcl-2 levels. The apoptotic cells increased from 5.2% in control to around 75% at 100 µM concentration. Mahanimbine also led to dose-dependent G0/G1 cell cycle arrest. Autophagic vacuoles appeared in the treated cells indicating autophagic induction by the test molecule. The Mahanimbine-triggered autophagy was also linked with increase in the expression of LC3II and decrease in p62 expression. However, no apparent effects were observed on the LC3 I expression. Conclusion: Taken together, the results of this study indicate that Mahanimbine natural product has the potential to be developed as a promising anticancer agent against human bladder carcinoma but further studies are needed to this direction.
Cytotoxicity of Mahanimbine from Curry Leaves in Human Breast Cancer Cells (MCF-7) via Mitochondrial Apoptosis and Anti-Angiogenesis
Molecules 2022 Feb 1;27(3):971.PMID:35164236DOI:10.3390/molecules27030971.
Mahanimbine (MN) is a carbazole alkaloid present in the leaves of Murraya koenigii, which is an integral part of medicinal and culinary practices in Asia. In the present study, the anticancer, apoptotic and anti-invasive potential of MN has been delineated in vitro. Apoptosis cells determination was carried out utilizing the acridine orange/propidium iodide double fluorescence test. During treatment, caspase-3/7,-8, and-9 enzymes and mitochondrial membrane potentials (Δψm) were evaluated. Anti-invasive properties were tested utilizing a wound-healing scratch test. Protein and gene expression studies were used to measure Bax, Bcl2, MMP-2, and -9 levels. The results show that MN could induce apoptosis in MCF-7 cells at 14 µM concentration IC50. MN-induced mitochondria-mediated apoptosis, with loss in Δψm, regulation of Bcl2/Bax, and accumulation of ROS (p ≤ 0.05). Caspase-3/7 and -9 enzyme activity were detected in MCF-7 cells after 24 and 48 h of treatment with MN. The anti-invasive property of MN was shown by inhibition of wound healing at the dose-dependent level and significantly suppressed mRNA and protein expression on MMP-2 and -9 in MCF-7 cells treated with a sub-cytotoxic dose of MN. The overall results indicate MN is a potential therapeutic compound against breast cancer as an apoptosis inducer and anti-invasive agent.