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| 10mg |
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| Targets |
Dehydrocorydaline (hydroxyl) has multiple molecular targets. It regulates apoptosis-related proteins by increasing the expression of the pro-apoptotic protein Bax (Bcl-2-associated X protein) and decreasing the expression of the anti-apoptotic protein Bcl-2 (B-cell lymphoma 2). It activates the initiator caspases-7 and -8, leading to the cleavage and inactivation of PARP (poly ADP-ribose polymerase). It also activates the p38 MAPK signaling pathway, which is involved in inflammation, myogenic differentiation, and cell survival. For its anti-malarial activity, it likely targets Plasmodium falciparum enzymes (unknown specific target).
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| ln Vitro |
Treatment with dehydrocorydaline hydroxy (0-200 μM) markedly and dose-dependently reduced the proliferation of MCF-7 cells. Cell viability was almost 40% lower after a 24-hour treatment with 200 μM dehydrocorydaline hydroxyl[1]. Dehydrocorydaline hydroxyl (0-200 μM) exhibits a dose-dependent increase in Bax protein expression and a decrease in Bcl-2 protein expression [1]. Without influencing caspase-9, dehydrocorydaline hydroxyl (0-200 μM) triggers the cleavage of PARP and the activation of caspase-7,-8[1].
In vitro, Dehydrocorydaline hydroxyl (0-200 microM) treatment significantly inhibits the growth of MCF-7 breast cancer cells in a dose-dependent manner. After 200 microM treatment for 24 hours, cell viability is reduced by approximately 40%. The compound dose-dependently increases Bax protein expression and decreases Bcl-2 protein expression. It induces activation of caspase-7 and -8 and cleavage of PARP without affecting caspase-9, indicating that it acts through the death receptor (extrinsic) apoptotic pathway rather than the mitochondrial (intrinsic) pathway. Dehydrocorydaline hydroxyl also shows strong anti-malarial effects against P. falciparum 3D7 strain with an IC50 of 38 nM, and it exhibits low cytotoxicity (cell viability > 90%) at anti-malarial concentrations. Additionally, it can enhance p38 MAPK activation, which contributes to its anti-inflammatory and anti-cancer effects. |
| ln Vivo |
Dehydrocorydaline hydroxy has a modest acute toxicity, with an intraperitoneal injection of 21.1±1.4 mg/kg and an oral LD50 of about 277.5±19.0 mg/kg body weight in mice[4].
In vivo, Dehydrocorydaline hydroxyl has been studied for its anti-nociceptive and anti-inflammatory effects. In mouse models of inflammatory pain (e.g., formalin test, acetic acid-induced writhing), it produces significant antinociception. The compound exhibits relatively low acute toxicity in mice, with an oral LD50 of approximately 277.5 +/- 19.0 mg/kg body weight and an intraperitoneal LD50 of 21.1 +/- 1.4 mg/kg. It has been shown to promote myogenic differentiation in vivo via p38 MAPK activation. Further in vivo studies would be required to evaluate its anti-tumor efficacy in xenograft models. No published human data exists for this research compound. |
| Enzyme Assay |
The p38 MAPK activation assay can be performed in cell lysates using a non-radioactive ELISA-based method or using Western blotting with phospho-specific antibodies. For Western blot analysis, cells (e.g., MCF-7 or C2C12 myoblasts) are treated with various concentrations of Dehydrocorydaline hydroxyl (0-200 microM) for 0-24 h. After treatment, cells are lysed in RIPA buffer containing protease and phosphatase inhibitors. Protein concentrations are determined by BCA assay. Equal amounts of protein (20-50 microg) are separated on 10-12% SDS-PAGE gels and transferred to PVDF membranes. The membranes are blocked with 5% BSA or non-fat milk and probed with primary antibodies against phospho-p38 MAPK (Thr180/Tyr182), total p38 MAPK, phospho-JNK, phospho-ERK1/2, phospho-caspase-7, -8, -3, PARP, Bax, Bcl-2, and beta-actin as a loading control. After incubation with HRP-conjugated secondary antibodies, signals are detected by enhanced chemiluminescence (ECL). Densitometric analysis is performed using ImageJ software. The ratio of phospho-p38 to total p38 is calculated to determine fold activation relative to controls. The IC50 value for growth inhibition is determined by curve fitting of cell viability data.
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| Cell Assay |
For anti-proliferative assays, MCF-7 human breast adenocarcinoma cells (or other cancer cell lines) are cultured in DMEM supplemented with 10% FBS, 100 U/mL penicillin, and 100 microg/mL streptomycin at 37degC in a 5% CO2 incubator. Cells are seeded in 96-well plates at 5 × 103 cells/well and incubated for 24 h. The medium is then replaced with fresh medium containing Dehydrocorydaline hydroxyl at concentrations of 0, 12.5, 25, 50, 100, and 200 microM (four replicate wells per concentration). After 24 h of treatment, cell viability is assessed by the MTT assay: 20 microL of MTT solution (5 mg/mL in PBS) is added to each well and incubated for 4 h at 37degC. The formazan crystals are dissolved in 150 microL of DMSO, and the absorbance at 570 nm is measured using a microplate reader. The inhibition rate is calculated as (1 - [ODtreated/ODcontrol]) × 100%. The IC50 value is calculated by non-linear regression. For apoptosis analysis, MCF-7 cells are treated with 0, 50, 100, or 200 microM of Dehydrocorydaline hydroxyl for 24 h. Cells are then harvested, washed with PBS, and stained with Annexin V-FITC and propidium iodide (PI) according to the manufacturer's instructions. The stained cells are analyzed by flow cytometry within 1 h. The percentage of apoptotic cells (early apoptotic: Annexin V+/PI-; late apoptotic: Annexin V+/PI+) is determined. For anti-malarial assays, P. falciparum 3D7 strain cultures are synchronized with sorbitol and incubated with the compound (0.1-1000 nM) for 48 h. [3H]hypoxanthine incorporation is measured to calculate IC50 values.
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| Animal Protocol |
In vivo antinociceptive activity is evaluated in adult male Kunming mice (18-22 g). For the acetic acid-induced writhing test, mice receive an intraperitoneal (i.p.) injection of 0.6% acetic acid (10 mL/kg). Dehydrocorydaline hydroxyl (dissolved in 0.5% CMC-Na) is administered orally at doses of 0, 50, 100, 200, and 400 mg/kg 30 min before the acetic acid injection. The number of writhes (abdominal constrictions) is counted for 15 min starting 5 min after acetic acid injection. For the formalin test, mice receive 20 microL of 2% formalin subcutaneously into the right hind paw. The licking time of the injected paw is recorded during the early phase (0-5 min, neurogenic pain) and the late phase (15-30 min, inflammatory pain). Dehydrocorydaline hydroxyl is administered orally 30 min before formalin injection. For acute toxicity testing, mice are observed for 14 days after a single oral or i.p. dose of Dehydrocorydaline hydroxyl. LD50 values are calculated using the Bliss method or Probit analysis. Signs of toxicity (e.g., salivation, convulsions, diarrhea, lethargy, mortality) are recorded. Body weight is measured daily. At the end of the study, major organs (liver, kidney, heart, lung, spleen) are examined for gross pathological changes.
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| ADME/Pharmacokinetics |
Pharmacokinetic data for Dehydrocorydaline hydroxyl is limited. It is an orally bioavailable alkaloid. Its high LD50 values (oral ~277 mg/kg in mice) suggest moderate systemic exposure. The compound likely undergoes hepatic metabolism, but no specific PK parameters (Cmax, Tmax, t½, AUC) have been reported in the literature. As a small molecule alkaloid with a molecular weight of approximately 383.44 g/mol, it is predicted to have moderate plasma protein binding and is likely eliminated by a combination of renal excretion and hepatic metabolism. The compound is soluble in DMSO and can be formulated for in vivo administration using vehicles such as 0.5% sodium carboxymethyl cellulose (CMC-Na). Its distribution to the central nervous system is plausible due to its ability to cross the blood-brain barrier (BBB), which is consistent with its observed antinociceptive effects.
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| Toxicity/Toxicokinetics |
The acute toxicity (LD50) of Dehydrocorydaline hydroxyl has been determined in mice. The oral LD50 is approximately 277.5 +/- 19.0 mg/kg body weight, and the intraperitoneal LD50 is approximately 21.1 +/- 1.4 mg/kg. These values indicate moderate toxicity via the oral route and higher toxicity via the intraperitoneal route, which is typical for many natural alkaloids. At sub-lethal oral doses (≤100 mg/kg), no significant adverse effects, body weight loss, or gross organ damage are observed. No chronic toxicity, genotoxicity, or carcinogenicity data have been reported for this specific hydroxyl form. Given the known toxicity profile of other protoberberine alkaloids (e.g., palmatine, berberine), hepatotoxicity is a potential concern at high chronic doses, although not specifically studied for Dehydrocorydaline hydroxyl. The compound's low cytotoxicity (cell viability > 90%) at effective anti-malarial concentrations (IC50 = 38 nM) suggests a favorable therapeutic window for anti-infective applications. Standard laboratory safety precautions should be followed. Avoid inhalation and skin contact. Wash hands thoroughly after handling. Dehydrocorydaline hydroxyl is for research use only, not for human or veterinary use.
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| References |
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| Additional Infomation |
Dehydrocorydaline (hydroxyl) is the hydroxylated form of Dehydrocorydaline, a quaternary protoberberine alkaloid originally isolated from the Chinese herb Corydalis yanhusuo (Yan Hu Suo), which is used in Traditional Chinese Medicine (TCM) for pain relief (analgesia) and promoting blood circulation. Dehydrocorydaline is one of the major active constituents in Corydalis species. This “hydroxyl” form likely refers to a specific derivative with enhanced solubility or altered biological properties. The compound's ability to activate p38 MAPK is linked to its promotion of myogenic differentiation, suggesting potential applications in muscle regeneration. Its strong anti-malarial activity (IC50 = 38 nM) is comparable to that of the standard drug chloroquine, indicating potential as a lead compound for development of new anti-malarials, especially against drug-resistant strains. Dehydrocorydaline hydroxyl's dual action on apoptosis (through death receptor pathway) and inflammation (through p38 MAPK modulation) makes it a versatile tool for studying cancer biology, inflammatory diseases, and parasitic infections. Dehydrocorydaline (hydroxyl) is for research use only; it is not a clinically approved drug. The compound should be stored at -20degC, protected from light and moisture, as a powder. It is soluble in DMSO and ethanol.
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| Molecular Formula |
C22H25NO5
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| Molecular Weight |
383.44
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| Related CAS # |
Dehydrocorydaline;30045-16-0;Dehydrocorydaline chloride;10605-03-5
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| Appearance |
Solid powder
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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 |
| 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) |
DMSO :~12.5 mg/mL (~32.60 mM)
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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 | 2.6080 mL | 13.0398 mL | 26.0797 mL | |
| 5 mM | 0.5216 mL | 2.6080 mL | 5.2159 mL | |
| 10 mM | 0.2608 mL | 1.3040 mL | 2.6080 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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