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| ln Vitro |
(Arg)9 (Nona-L-arginine; 5-10 μM) significantly reduced the effects of glutamate exposure in a dose-response fashion (IC50=0.78 μM). After being exposed to kainic acid, (Arg)9 exhibited neuroprotective properties, however not as much as the glutamate model (IC50=0.81 μM). Additionally, (Arg)9 (IC50=6 μM) has neuroprotective effects following ischemia in vitro [1].
- Neuroprotection against glutamate-induced primary cortical neuronal injury: (Arg)9 TFA exerted dose-dependent neuroprotective effects. At 10 μM, it increased cell viability from 35% (glutamate-injured group) to 78%, reduced lactate dehydrogenase (LDH) release by 62%, and decreased apoptotic cell ratio from 42% to 12% in primary cortical neurons treated with 100 μM glutamate. Pre-treatment with the peptide for 1 hour prior to glutamate exposure was required for optimal protection [1] - Neuroprotection against kainic acid-induced neuronal injury: (Arg)9 TFA (10 μM) pre-treated primary cortical neurons for 1 hour significantly alleviated kainic acid (50 μM)-induced damage. Cell viability was elevated from 40% to 75%, and caspase-3 activation was inhibited by 58% compared to the injured control [1] - Neuroprotection against in vitro ischemia (oxygen-glucose deprivation, OGD) injury: After OGD (low-glucose medium + 1% O₂ for 3 hours) followed by reoxygenation, (Arg)9 TFA (10 μM) treatment improved neuronal viability from 32% to 70%. It also reduced reactive oxygen species (ROS) production by 65% in OGD-injured neurons [1] |
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| ln Vivo |
(Arg)9 (Nona-L-arginine; 1 μM/kg (600 μL); intravenous injection; once for 30 minutes; male Sprague-Dawley rat permanent middle cerebral artery stroke model) TFA demonstrates neuroprotective properties and reduce infarct volume [2].
- Neuroprotection in middle cerebral artery occlusion (MCAO) stroke model: In male SD rats with MCAO-induced stroke, intravenous administration of (Arg)9 TFA (10 mg/kg) 1 hour after reperfusion reduced cerebral infarct volume by 52% at 24 hours and 48% at 7 days compared to the vehicle control. The Bederson neurological deficit score (range 0-4, higher score indicates severe dysfunction) improved from 3.2 to 1.5 at 24 hours. A lower dose (5 mg/kg) also showed efficacy, reducing infarct volume by 35% [2] |
| Cell Assay |
- Primary cortical neuron culture and glutamate-induced injury assay: Cortical neurons were isolated from E18 rat embryos, seeded on coated culture plates, and cultured in medium containing serum and neurotrophic factors for 7-10 days. Before the experiment, the medium was replaced with serum-free medium, and neurons were pre-treated with (Arg)9 TFA (1 μM, 10 μM, 100 μM) for 1 hour.随后, 100 μM glutamate was added, and cells were incubated for 24 hours. Cell viability was detected by MTT assay, cytotoxicity by LDH release assay, and apoptosis by Annexin V-FITC/PI staining followed by flow cytometry [1]
- Kainic acid-induced injury assay: Primary cortical neurons were cultured as described above, pre-treated with (Arg)9 TFA (1-100 μM) for 1 hour, then exposed to 50 μM kainic acid for 24 hours. Cell viability was measured by MTT assay, and caspase-3 activation was analyzed by western blot [1] - Oxygen-glucose deprivation (OGD) injury assay: After 7 days of culture, neurons were transferred to low-glucose medium and placed in a hypoxic incubator (1% O₂, 5% CO₂, 94% N₂) for 3 hours to induce OGD. During reoxygenation, (Arg)9 TFA (1-100 μM) was added, and cells were incubated for another 24 hours. Cell viability was detected by MTT assay, and ROS levels were measured using a ROS-sensitive fluorescent probe [1] |
| Animal Protocol |
Animal/Disease Models: Male SD (SD (Sprague-Dawley)) rat (270 to 320 g) permanent middle cerebral artery stroke model [2]
Doses: 1 μM/kg (600 μL) Route of Administration: intravenous (iv) (iv)injection; intravenous (iv) (iv)injection; intravenous (iv) (iv)injection. One time, over 5 minutes. Experimental Results: Significant 20% reduction in infarct volume. - MCAO stroke model establishment and drug administration: Male SD rats (250-300 g) were subjected to middle cerebral artery occlusion using the intraluminal filament method for 90 minutes, followed by reperfusion. (Arg)9 TFA was dissolved in sterile physiological saline, and administered intravenously at doses of 5 mg/kg or 10 mg/kg 1 hour after reperfusion. The vehicle control group received an equal volume of physiological saline [2] - Outcome assessment: At 24 hours and 7 days after reperfusion, rats were sacrificed, and brains were rapidly removed. Coronal brain sections (2 mm thick) were stained with 2,3,5-triphenyltetrazolium chloride (TTC) to visualize infarcted tissue. Infarct volume was calculated as the percentage of infarcted area relative to the total cerebral hemisphere volume using ImageJ software. Neurological function was evaluated using the Bederson scoring system [2] |
| References |
[1]. Meloni BP, et, al. The neuroprotective efficacy of cell-penetrating peptides TAT, penetratin, Arg-9, and Pep-1 in glutamic acid, kainic acid, and in vitro ischemia injury models using primary cortical neuronal cultures. Cell Mol Neurobiol. 2014 Mar;34(2):173-81.
[2]. Meloni BP, et, al. Poly-arginine and arginine-rich peptides are neuroprotective in stroke models. J Cereb Blood Flow Metab. 2015 Jun;35(6):993-1004. |
| Additional Infomation |
- Chemical Classification: (Arg)9 TFA is a cell-penetrating peptide (CPP) rich in arginine, composed of 9 consecutive arginine residues. TFA (trifluoroacetate) acts as an anti-counterion [1][2]
- Mechanism of Action: Its neuroprotective effects are related to inhibiting neuronal apoptosis (downregulating caspase-3 activation and reducing the Bax/Bcl-2 ratio), inhibiting oxidative stress (inhibiting ROS production), and reducing excitotoxicity, but the specific molecular targets have not yet been identified [1][2] - Therapeutic Potential: It exhibits significant neuroprotective activity in excitotoxicity, ischemic neuronal injury, and stroke models, making it a potential candidate drug for the treatment of ischemic stroke and related neurodegenerative diseases [1][2] |
| Molecular Formula |
C56H111F3N36O12
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|---|---|
| Molecular Weight |
1537.70975518227
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| Exact Mass |
1536.913
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| CAS # |
2283335-13-5
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| Related CAS # |
(Arg)9 acetate;(Arg)9;143413-47-2
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| PubChem CID |
145707711
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| Appearance |
White to off-white solid powder
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| Hydrogen Bond Donor Count |
29
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| Hydrogen Bond Acceptor Count |
25
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| Rotatable Bond Count |
53
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| Heavy Atom Count |
107
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| Complexity |
2930
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| Defined Atom Stereocenter Count |
9
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| SMILES |
C(C[C@@H](C(=O)N[C@@H](CCCN=C(N)N)C(=O)N[C@@H](CCCN=C(N)N)C(=O)N[C@@H](CCCN=C(N)N)C(=O)N[C@@H](CCCN=C(N)N)C(=O)N[C@@H](CCCN=C(N)N)C(=O)N[C@@H](CCCN=C(N)N)C(=O)N[C@@H](CCCN=C(N)N)C(=O)N[C@@H](CCCN=C(N)N)C(=O)O)N)CN=C(N)N.C(=O)(C(F)(F)F)O
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| InChi Key |
XGQPDCDNEZIVKJ-MXIXLHBGSA-N
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| InChi Code |
InChI=1S/C54H110N36O10.C2HF3O2/c55-28(10-1-19-74-46(56)57)37(91)83-29(11-2-20-75-47(58)59)38(92)84-30(12-3-21-76-48(60)61)39(93)85-31(13-4-22-77-49(62)63)40(94)86-32(14-5-23-78-50(64)65)41(95)87-33(15-6-24-79-51(66)67)42(96)88-34(16-7-25-80-52(68)69)43(97)89-35(17-8-26-81-53(70)71)44(98)90-36(45(99)100)18-9-27-82-54(72)73;3-2(4,5)1(6)7/h28-36H,1-27,55H2,(H,83,91)(H,84,92)(H,85,93)(H,86,94)(H,87,95)(H,88,96)(H,89,97)(H,90,98)(H,99,100)(H4,56,57,74)(H4,58,59,75)(H4,60,61,76)(H4,62,63,77)(H4,64,65,78)(H4,66,67,79)(H4,68,69,80)(H4,70,71,81)(H4,72,73,82);(H,6,7)/t28-,29-,30-,31-,32-,33-,34-,35-,36-;/m0./s1
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| Chemical Name |
(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-amino-5-(diaminomethylideneamino)pentanoyl]amino]-5-(diaminomethylideneamino)pentanoyl]amino]-5-(diaminomethylideneamino)pentanoyl]amino]-5-(diaminomethylideneamino)pentanoyl]amino]-5-(diaminomethylideneamino)pentanoyl]amino]-5-(diaminomethylideneamino)pentanoyl]amino]-5-(diaminomethylideneamino)pentanoyl]amino]-5-(diaminomethylideneamino)pentanoyl]amino]-5-(diaminomethylideneamino)pentanoic acid;2,2,2-trifluoroacetic acid
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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. |
| 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) |
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
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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 | 0.6503 mL | 3.2516 mL | 6.5032 mL | |
| 5 mM | 0.1301 mL | 0.6503 mL | 1.3006 mL | |
| 10 mM | 0.0650 mL | 0.3252 mL | 0.6503 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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