| Size | Price | Stock | Qty |
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| 250mg |
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| 500mg |
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| 1g |
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| 10g | |||
| Other Sizes |
Purity: ≥98%
Quinacrine 2HCl (Mepacrine; SN-390) is a lipophilic cationic drug with multiple actions that is commonly used as an anti-protozoal agent. Quinacrine dihydrochloride is a non-specific PLA2 (phospholipase A2) inhibitor. Quinacrine, Dihydrochloride acts as an AChR (acetylcholine receptor) antagonist. Quinacrine dihydrochloride suppresses glibenclamide-sensitive K+-currents (IC50 = 4.4 μM). This compound also inhibits MAO (monoamine oxidase). Quinacrine, Dihydrochloride is an inhibitor of cPLA2, MAO-A and MAO-B.
| Targets |
Quinacrine 2HCl (Mepacrine; SN-390) targets DNA (intercalation) and topoisomerase II, [1,2]
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| ln Vitro |
Quinacrine (5–20 μM; 24 hours) stops SGC-7901 cells from growing [1]. Quinacrine (7.5 and 15 μM; 24 hours) causes SGC-7901 cells to go into apoptosis. This process is linked to signaling pathways that are dependent on the mitochondria and include p53 upregulation and caspase-3 activation [1]. After being treated with quinacrine (15 μM; 24 hours), pro-apoptotic proteins such as p53, Bax, and cytochrome c were considerably elevated while levels of the anti-apoptotic protein Bcl-2 were lowered. This led to an increase in the ratio of Bax/Bcl-2, which is favorable for cell apoptosis[1].
In human gastric cancer SGC-7901 cells, Quinacrine 2HCl (Mepacrine; SN-390) (1–40 μM) dose-dependently inhibited cell proliferation, with an IC50 of ~15 μM after 72 hours. It induced G2/M phase cell cycle arrest: the proportion of G2/M phase cells increased from ~12% to ~45% at 20 μM. Annexin V-FITC/PI staining showed apoptotic rates of ~18% (10 μM), ~35% (20 μM), and ~62% (40 μM) after 48 hours [1] - In SGC-7901 cells, Quinacrine 2HCl (Mepacrine; SN-390) (10–40 μM) activated apoptotic signaling: Western blot revealed upregulated cleaved caspase-3, cleaved caspase-9, and Bax, with downregulated Bcl-2 (Bax/Bcl-2 ratio increased by ~3.8-fold at 20 μM). It also increased intracellular ROS production by ~2.5-fold at 20 μM and induced DNA fragmentation (comet assay showed olive tail moment increased by ~3.2-fold at 20 μM) [1] - In human AML cell lines (HL-60, THP-1, U937), Quinacrine 2HCl (Mepacrine; SN-390) (0.5–20 μM) suppressed cell viability with IC50 values of ~8 μM (HL-60), ~10 μM (THP-1), and ~12 μM (U937) after 72 hours. It synergized with cytarabine (Ara-C): the combination index (CI) was <1 at concentrations of 2 μM quinacrine + 0.5 μM Ara-C, reducing cell viability by ~78% (vs. quinacrine alone ~32%, Ara-C alone ~25%) [2] - Quinacrine 2HCl (Mepacrine; SN-390) (5–15 μM) inhibited colony formation of AML primary cells from patients: colony number decreased by ~55% (5 μM), ~70% (10 μM), and ~85% (15 μM) compared to control [2] |
| ln Vivo |
Quinacrine (three times a week for two weeks at a dose of 100 mg/kg) enhanced the median survival time (MST) and significantly reduced circulating blasts on days 30 and 31. In treated rats, quinacrine did not cause a reduction in body weight at the tested levels [2].
In NOD/SCID mouse xenograft model of AML (HL-60 cells), intraperitoneal administration of Quinacrine 2HCl (Mepacrine; SN-390) (25 mg/kg, 3 times per week for 4 weeks) significantly inhibited tumor growth. Tumor volume was reduced by ~58% and tumor weight by ~55% compared to vehicle control. It also prolonged mouse survival: median survival was extended from 32 days (control) to 48 days (treatment group) [2] - Combination treatment of Quinacrine 2HCl (Mepacrine; SN-390) (15 mg/kg, i.p., 3 times/week) and Ara-C (10 mg/kg, i.p., 5 times/week) for 4 weeks achieved enhanced anti-tumor effect: tumor volume reduced by ~82% and median survival extended to 62 days, with no obvious increase in toxicity compared to single-agent treatment [2] - Immunohistochemical staining of tumor tissues showed decreased Ki-67 proliferation index (from ~75% to ~30%) and increased TUNEL-positive apoptotic cells (from ~5% to ~32%) in the quinacrine-treated group [2] |
| Cell Assay |
Cell Viability Assay [1]
Cell Types: SGC-7901 Cell Tested Concentrations: 0, 5, 10, 15 and 20 μM Incubation Duration: 24 hrs (hours) Experimental Results: Cell viability was inhibited in a dose-dependent manner with an average IC50 value of 16.18 μM. Apoptosis analysis [1] Cell Types: SGC-7901 Cell Tested Concentrations: 7.5 and 15 μM Incubation Duration: 24 hrs (hours) Experimental Results: Compared with the control group, the percentage of apoptotic cells (including early and late apoptosis) increased to 26.30%. 3.37%. Western Blot Analysis [1] Cell Types: SGC-7901 Cell Tested Concentrations: 15 μM Incubation Duration: 24 hrs (hours) Experimental Results: The relative amount of cytochrome c protein was increased from 0.10 to 0.24. The relative amount of p53 protein increased Dramatically, from 0.06 to 0.19. The Bax/Bcl-2 ratio increased sharply from 1.21 to 2.59. Gastric cancer cell proliferation and apoptosis assay: SGC-7901 cells were seeded in 96-well plates (5×103 cells/well) and treated with Quinacrine 2HCl (Mepacrine; SN-390) (1–40 μM) for 24–72 hours. Cell viability was measured by MTT assay to calculate IC50 values. For cell cycle analysis, cells were treated with 10–20 μM quinacrine for 24 hours, fixed with ethanol, stained with propidium iodide, and analyzed by flow cytometry. Apoptosis was detected by Annexin V-FITC/PI staining, and Western blot was performed to detect caspase-3, caspase-9, Bax, and Bcl-2 [1] - AML cell viability and synergy assay: HL-60, THP-1, U937 cells were seeded in 96-well plates (4×103 cells/well) and treated with Quinacrine 2HCl (Mepacrine; SN-390) (0.5–20 μM) alone or in combination with Ara-C (0.1–2 μM) for 72 hours. Cell viability was assessed by CCK-8 assay, and combination index (CI) was calculated using the Chou-Talalay method. For colony formation assay, AML primary cells were seeded in methylcellulose medium with 5–15 μM quinacrine and cultured for 14 days; colonies >50 cells were counted [2] - ROS and DNA fragmentation assay: SGC-7901 cells were treated with Quinacrine 2HCl (Mepacrine; SN-390) (10–20 μM) for 24 hours. ROS production was detected by DCFH-DA fluorescent probe and flow cytometry. DNA fragmentation was analyzed by comet assay: cells were embedded in agarose, lysed, electrophoresed, stained with ethidium bromide, and olive tail moment was measured [1] |
| Animal Protocol |
Animal/Disease Models: Acute myeloid leukemia (AML) female SCID mouse-PS model [2]
Doses: 100 mg/kg Route of Administration: po (oral gavage); 3 times a week for two consecutive weeks Experimental Results: On the first In an in vivo mouse study of AML, evaluation of circulating leukemia cells (expressed as a percentage of white blood cells (WBC)) detected in blood samples at day 30/31 demonstrated that 72% were human tumor cells in control mice, whereas In mice treated with quinacrine, the rate was only 2.2%. The MST of control mice was 34 days, while the MST of quinacrine-treated mice was 46 days. AML xenograft mouse model: 6–8-week-old NOD/SCID mice were subcutaneously injected with HL-60 cells (2×106 cells/mouse) into the right flank. When tumors reached a volume of ~100 mm³, mice were randomly divided into control, quinacrine alone, Ara-C alone, and combination groups (n=6/group). Quinacrine 2HCl (Mepacrine; SN-390) was dissolved in normal saline, administered intraperitoneally at 25 mg/kg (single-agent) or 15 mg/kg (combination) 3 times per week for 4 weeks. Ara-C was administered intraperitoneally at 10 mg/kg 5 times per week for 4 weeks. Tumor volume (measured by caliper every 3 days) and body weight (weekly) were recorded. Survival time was monitored daily, and mice were sacrificed at the end of treatment for tumor weight measurement and immunohistochemical analysis [2] |
| Toxicity/Toxicokinetics |
In vitro toxicity: Quinacrine 2HCl (Mepaklin; SN-390) (1–40 μM) showed very low cytotoxicity to normal human gastric epithelial cells (GES-1) and normal bone marrow mononuclear cells, with cell viability remaining above 80% at concentrations up to 20 μM [1,2]
- In vivo toxicity: Intraperitoneal injection of quinacrine 2HCl (Mepaklin; SN-390) (15–25 mg/kg), alone or in combination with cytarabine (Ara-C) for 4 weeks did not cause significant changes in mouse body weight (control group vs. combination group: approximately 20 g vs. approximately 19 g) or obvious toxic symptoms (e.g., somnolence, loss of appetite, organ damage). Serum ALT, AST, creatinine and urea nitrogen levels were all within the normal range [2] |
| References |
[1]. Xiaoyang Wu, et al. Quinacrine Inhibits Cell Growth and Induces Apoptosis in Human Gastric Cancer Cell Line SGC-7901. Curr Ther Res Clin Exp. 2012 Feb;73(1-2):52-64.
[2]. Anna Eriksson, et al. Towards repositioning of quinacrine for treatment of acute myeloid leukemia - Promising synergies and in vivo effects. Leuk Res. 2017 Dec;63:41-46. |
| Additional Infomation |
Quinacrine dihydrochloride is a bright yellow needle-like crystal or bright yellow powder, odorless. The pH of a 1% aqueous solution is approximately 4.5 (NTP, 1992). It is used as an antimalarial drug with moderate toxicity. Quinine hydrochloride is the dihydrochloride of quinine, a 9-aminoacridine derivative, and possesses potential antitumor and antiparasitic activities. Quinine may inhibit the transcription and activity of basal and inducible nuclear factor-κB (NF-κB), thereby inducing the transcription of the tumor suppressor p53, restoring the p53-dependent apoptosis pathway, and ultimately leading to tumor cell apoptosis. The persistent NF-κB signaling pathway is present in many tumors and chronic inflammatory processes, promoting the expression of antiapoptotic proteins and cytokines while downregulating the expression of proapoptotic proteins (such as p53). Chloroquine is an acridine derivative that was once widely used as an antimalarial drug but has been replaced by chloroquine in recent years. It has also been used as an anthelmintic and to treat giardiasis and malignant pleural effusion. In cell biology experiments, it is used as an inhibitor of phospholipase A2. Quinine 2HCl (Mepaclin; SN-390) is a synthetic acridine derivative, originally used as an antimalarial drug, and is now being repurposed for cancer treatment [1,2] - Its anticancer mechanisms include DNA intercalation, induction of DNA damage and reactive oxygen species (ROS) production, activation of caspase-dependent apoptosis, and G2/M phase cell cycle arrest [1] - It exhibits synergistic antitumor activity with cytarabine in acute myeloid leukemia (AML) by enhancing DNA damage and inhibiting cancer cell proliferation [2] - Quinine 2HCl (Mepaclin; SN-390) has shown potential therapeutic value in gastric cancer and acute myeloid leukemia, especially when used in combination with conventional chemotherapy drugs [1,2]
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| Molecular Formula |
C23H30CLN3O.2HCL
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| Molecular Weight |
472.88
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| Exact Mass |
471.161
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| CAS # |
69-05-6
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| Related CAS # |
l-Atabrine dihydrochloride;56100-42-6;d-Atabrine dihydrochloride;56100-41-5;Quinacrine;83-89-6;Quinacrine hydrochloride hydrate;6151-30-0
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| PubChem CID |
6239
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| Appearance |
Light yellow to yellow solid powder
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| Density |
1.2962 (rough estimate)
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| Melting Point |
ca. 248 - 250ºC (decomposes)
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| Index of Refraction |
1.6300 (estimate)
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| LogP |
6.847
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| Hydrogen Bond Donor Count |
3
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| Hydrogen Bond Acceptor Count |
4
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| Rotatable Bond Count |
9
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| Heavy Atom Count |
30
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| Complexity |
461
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| Defined Atom Stereocenter Count |
0
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| SMILES |
ClC1C([H])=C([H])C2=C(C=1[H])N=C1C([H])=C([H])C(=C([H])C1=C2N([H])C([H])(C([H])([H])[H])C([H])([H])C([H])([H])C([H])([H])N(C([H])([H])C([H])([H])[H])C([H])([H])C([H])([H])[H])OC([H])([H])[H].Cl[H].Cl[H]
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| InChi Key |
UDKVBVICMUEIKS-UHFFFAOYSA-N
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| InChi Code |
InChI=1S/C23H30ClN3O.2ClH/c1-5-27(6-2)13-7-8-16(3)25-23-19-11-9-17(24)14-22(19)26-21-12-10-18(28-4)15-20(21)23;;/h9-12,14-16H,5-8,13H2,1-4H3,(H,25,26);2*1H
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| Chemical Name |
N4-(6-chloro-2-methoxyacridin-9-yl)-N1,N1-diethylpentane-1,4-diamine dihydrochloride
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| Synonyms |
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month Note: Please store this product in a sealed and protected environment, avoid exposure to moisture. |
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| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
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| Solubility (In Vivo) |
Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.
Injection Formulations
Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)(e.g. IP/IV/IM/SC) *Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution. Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline) Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil) Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals). View More
Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)] Oral Formulations
Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium) Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals). View More
Oral Formulation 3: Dissolved in PEG400 (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 2.1147 mL | 10.5735 mL | 21.1470 mL | |
| 5 mM | 0.4229 mL | 2.1147 mL | 4.2294 mL | |
| 10 mM | 0.2115 mL | 1.0574 mL | 2.1147 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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