In frogs, Magnocurarine (0.25 mg/10g body weight) weakened the righting reaction; 0.5 mg/10g abolished the righting reaction but weak reflex contraction and respiratory movements remained; 0.75 mg/10g caused complete cessation of all movements including respiration, though the heart continued beating. The paralysis induced by 0.75 mg and 1.0 mg of Magnocurarine persisted for 165 and 330 minutes, respectively. d-Tubocurarine was approximately ten times more potent than Magnocurarine based on effective doses in the righting reaction. [1]
In frogs, neuromuscular blocking action was confirmed: after injection of 0.75 mg/10g Magnocurarine into the lymph sac, the contractile response of the gastrocnemius muscle to nerve stimulation was gradually depressed and completely disappeared 25 minutes post-administration, while the drug-free contralateral muscle showed no depression. The drug had no direct effect on muscle or nerve, as the paralyzed muscle responded fully to direct electrical stimulation. [1]
In frogs, Magnocurarine (1 mg) showed no depressive effect on the spinal multineuron reflex (strychnine-pretreated preparation), unlike myanesin which blocked the reflex. [1]
In mice, intraperitoneal injection of lethal doses of Magnocurarine caused limpness, inability to walk, head drop, respiratory arrest within 3-5 minutes, and finally cardiac cessation after mild convulsion. The LD50 per 10g body weight was 0.455 mg. Sublethal doses caused limb paralysis lasting 40-50 minutes. [1]
In mice, using a single fast intravenous injection (5 seconds), the head drop dose of Magnocurarine was 0.107 mg/10g, the lethal dose was 0.243 mg/10g, and the LD50 was 0.0843 mg/10g. The margin of safety (lethal dose/head drop dose) was approximately 2.2 for Magnocurarine (slow injection) and 2.1 (fast injection), compared to 2.6 and 1.85 for C10. [1]
In rabbits, intravenous administration of 5 mg/kg Magnocurarine decreased gastrocnemius muscle response to nerve stimuli for 5-8 minutes, with early respiratory depression followed by stimulation for 8-10 minutes. At 10 mg/kg, the inhibition and respiratory effects were more marked and longer-lasting. At 15 mg/kg, contractile response was completely abolished within 1 minute, and respiratory movements ceased; after artificial respiration, muscle response and spontaneous respiration began to recover in 7-8 minutes, with full recovery in 25-30 minutes. [1]

For frog experiments, Magnocurarine was dissolved in water and injected into the ventral lymph sac. The onset of ataxia, limb paralysis, and duration were examined. Neuromuscular blockade was determined by faradization of muscle and sciatic nerve, and in some experiments one leg was ligated by Claude-Bernard's method. A single shock from a Du Bois-Reymond inductorium was used for nerve stimulation. [1]
For mouse acute toxicity, Magnocurarine solution (1 mg/1 ml) was injected intraperitoneally. For head drop and lethal dose determination, a prolonged slow injection assay method was used: mice received 0.025 mg of Magnocurarine every 15 seconds into the tail vein until head drop occurred. For single fast injection, the total dose was administered in 5 seconds. [1]
For rabbit head drop assay, Magnocurarine (2 mg) was injected in 15 seconds into the marginal ear vein of restrained rabbits (2.0-2.5 kg) until head drop occurred. For muscle contraction and respiration studies, rabbits were anesthetized with urethane (1 g/kg body weight). Magnocurarine was injected into the marginal ear vein in 5 seconds. The trachea was cannulated and connected to a tambour, and the gastrocnemius muscle was attached to an isometric lever. The sciatic nerve was stimulated with a single shock at 18 impulses per minute. Muscle contraction and respiratory movements were simultaneously recorded on a kymograph. [1]

In mice, intraperitoneal LD50 of Magnocurarine was 0.455 mg per 10g body weight. [1]
In mice, intravenous head drop dose (slow injection, 0.025 mg/15 sec) was 0.107 mg/10g; lethal dose was 0.243 mg/10g; LD50 (single fast injection over 5 sec) was 0.0843 mg/10g. The margin of safety (lethal/head drop) was approximately 2.2 for slow injection and 2.1 for fast injection. [1]
In rabbits, intravenous head drop dose (2 mg/15 sec) was 15.63 mg/kg. [1]

[1]. Curare-like action of magnocurarine, isolated from Magnolia obovata[J]. The Japanese Journal of Pharmacology, 1953, 2(2): 89-96.

[2]. Neuromuscular blocking action of alkaloids from a Japanese crude drug “Shin-I”(Flos Magnoliae) in frog skeletal muscle[J]. Planta medica, 1983, 48(05): 43-47.

[3]. (R)-Magnocurarine from Evodia cf. trichotoma. Planta Med. 1993 Jun;59(3):290.

Magnocurarine belongs to the isoquinoline class of compounds. It has been reported to exist in Gnetum montanum, Lindera megaphylla, and other organisms with relevant data.

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Magnocurarine chloride was compared with d-tubocurarine chloride and decamethonium iodide (C10). In frogs, d-tubocurarine chloride was ten times as potent as Magnocurarine chloride. In mice, the duration of curarizing effect of a moderate dose of C10 was slightly longer than that of Magnocurarine. In rabbits, 0.1 mg/kg C10 completely abolished muscle response for 7 minutes with relatively spared respiration, whereas 15 mg/kg Magnocurarine caused simultaneous respiratory arrest. [1]

C19H24NO3

314.3988

314.175

6801-40-7

(Rac)-Magnocurarin chloride; 2365275-47-2

53266

Typically exists as solid at room temperature

199-200 ºC

-1.91

2

3

3

23

392

1

O(C([H])([H])[H])C1=C(C([H])=C2C(=C1[H])C([H])([H])C([H])([H])[N+](C([H])([H])[H])(C([H])([H])[H])[C@]2([H])C([H])([H])C1C([H])=C([H])C(=C([H])C=1[H])O[H])O[H]

CLWOXNLVWMXBRD-QGZVFWFLSA-O

InChI=1S/C19H23NO3/c1-20(2)9-8-14-11-19(23-3)18(22)12-16(14)17(20)10-13-4-6-15(21)7-5-13/h4-7,11-12,17H,8-10H2,1-3H3,(H-,21,22)/p+1/t17-/m1/s1

(1R)-1-[(4-hydroxyphenyl)methyl]-6-methoxy-2,2-dimethyl-3,4-dihydro-1H-isoquinolin-2-ium-7-ol

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples

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.

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Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)
*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).

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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)]
*Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.
Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin → 500 μL Saline)
Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO → 100 μLPEG300 → 200 μL castor oil → 650 μL Saline)
Injection Formulation 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (i.e. 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline
Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH → 900 μL Corn oil)
Injection Formulation 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)

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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).

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Oral Formulation 3: Dissolved in PEG400
Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose
Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose
Oral Formulation 6: Mixing with food powders

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Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently.

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 (Please use freshly prepared in vivo formulations for optimal results.)