N-Acetyl-L-tryptophan
Based on 1 Customer Validation
N-Acetyl-L-tryptophan is an antagonist of the neurokinin-1 receptor (NK-1R), disrupting the binding of substance P (SP) to NK-1R. This action provides neuroprotective effects, improving memory deficits and motor impairments. N-Acetyl-L-tryptophan is also an inhibitor of cytochrome c (Cytochrome c), and it exerts antioxidant and anti-inflammatory effects by inhibiting the expression of IL-1β and the activation of caspase-1. N-Acetyl-L-tryptophan holds promise for research in neurodegenerative and inflammatory diseases.
For research use only. We do not sell to patients.
- Purity : 99.82%
- CAS No.: 1218-34-4
- Formula: C13H14N2O3
- Molecular Weight:246.26
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Storage:Powder -20°C, 3 years , 4°C, 2 years ; In solvent -80°C, 6 months , -20°C, 1 month
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biological Activity
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Chemical Information
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Solvent & Solubility
- Protocols
- Purity & Documentation
- References
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Help & FAQs
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HY-N0623
L-TryptophanEssential Amino Acid -
HY-W012980
Isovaleric acidAMPK Activator -
HY-101047
D-erythro-SphingosinePKC Inhibitor -
HY-B2156
Menaquinone-4Endogenous Metabolite -
HY-N4075
O-DesmethylangolensinEndogenous Metabolite -
HY-W020215
Tricarballylic acidAconitate Hydratase Inhibitor -
HY-W017158
Melilotic acidOrally Active Compound -
HY-W011978R
N-Acetyl-L-tryptophan (Standard) -
HY-W011982
Ac-DL-Trp-OH -
HY-W012480
DL-TryptophanAhR Activator -
HY-10053
MaropitantNK1 Receptor Antagonist -
HY-W011982R
Ac-DL-Trp-OH (Standard)
Biological Activity
Description
IC50 & Target
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Microbial Metabolite |
Human Endogenous Metabolite |
NK1R |
Caspase-1 |
IL-1β |
In Vitro
N-Acetyl-L-tryptophan (0.001–10 nM, 0.1–300 µM, 2 h) exhibits neuroprotective effects in a H2O2-induced amyotrophic lateral sclerosis model (cell lines: NSC-34 motoneurons and primary motor neurons.) induced by H2O2[1]. N-Acetyl-L-tryptophan (30 μM, 15 min-6 h) inhibits the secretion of Substance P (HY-P0201) and lL-1β and the activation of caspase-1 in NSC-34 motoneurons[1]. N-Acetyl-L-tryptophan (10 μM, 2 h) inhibits cell death in a H2O2-induced amyotrophic lateral sclerosis model by preventing the release of cytochrome c, Smac, and AIF from the mitochondria[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:H2O2-induced amyotrophic lateral sclerosis model (NSC-34 motoneurons and Primary motor neurons)
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Concentration:0.001, 0.01, 0.1, 1, 10 nM, 0.1, 1, 10, 30, 200, 300 μM
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Incubation Time:2 h
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Result:Significantly inhibited H2O2-induced cell death in NSC-34 motoneurons and primary motor neurons, with IC50 values of 0.3 µM and 16 nM, respectively.
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Cell Line:H2O2-induced amyotrophic lateral sclerosis model (NSC-34 motoneurons)
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Concentration:10 μM
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Incubation Time:2 h
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Result:Effectively inhibited the release of cytochrome c/Smac/AIF from mitochondria into the cytoplasm.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Ischemia-reperfusion-induced liver injury model in Sprague-Dawley (SD) rats (200-220 g)[2]
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Dosage:10 mg/kg
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Administration:Intraperitoneal injection (i.p.), single dose
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Result:Reduced the expression of autophagy markers (Beclin1, LC3-II, ATG-7, and P62) in the ischemia-reperfusion-induced Sprague-Dawley (SD) rat liver injury model.
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Animal Model:L-DOPA (HY-N0304)-induced abnormal involuntary movements model in Spraguee Dawley rats(230-270 g, before L-DOPA induction, a hemi-parkinsonian model was created by Oxidopamine hydrobromide (HY-B1081A))
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Dosage:0.5 mg/kg
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Administration:Subcutaneous injection (s.c.), once daily for 21 days
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Result:Significantly reduced the onset of dyskinesia.
Chemical Information
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CAS No. 1218-34-4
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Appearance Solid
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Molecular Weight 246.26
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Formula C13H14N2O3
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Color White to off-white
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SMILES
O=C(O)[C@H](CC1=CNC2=C1C=CC=C2)NC(C)=O
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Structure Classification
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Initial Source
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month
Solvent & Solubility
In Vitro:
DMSO : 100 mg/mL (406.07 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
In Vivo:
Select the appropriate dissolution method based on your experimental animal and administration route.
- For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
- To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for In Vivo experiments, it is recommended to prepare freshly and use it on the same day.
- The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.
Add each solvent one by one: 10% DMSO 40% PEG300 5% Tween-80 45% Saline
Solubility: ≥ 2.5 mg/mL (10.15 mM); Clear solution
This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown).
Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 mg/mL) to 400 μL PEG300, and mix evenly; then add 50 μL Tween-80 and mix evenly; then add 450 μL Saline to adjust the volume to 1 mL.
Preparation of Saline: Dissolve 0.9 g sodium chloride in ddH₂O and dilute to 100 mL to obtain a clear Saline solution.
Add each solvent one by one: 10% DMSO 90% (20% SBE-β-CD in Saline)
Solubility: ≥ 2.5 mg/mL (10.15 mM); Clear solution
This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown).
Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 mg/mL) to 900 μL 20% SBE-β-CD in Saline, and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C, storage for one week): 2 g SBE-β-CD powder is dissolved in 10 mL Saline, completely dissolve until clear.
In Vivo Dissolution Calculator
Please enter the basic information of animal experiments:
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Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.
Please enter your animal formula composition:
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%DMSO +
Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
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%+
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+%Tween-80 + +
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%Saline +
The co-solvents required include: DMSO, . All of co-solvents are available by MedChemExpress (MCE). , Tween 80. All of co-solvents are available by MedChemExpress (MCE).
Working solution concentration: 0.22 mg/mL
Method for preparing stock solution: mg drug dissolved in μL DMSO. Stock solution concentration: mg/mL.
1. Take μL DMSO stock solution;
2. Add μL .
μL , mix evenly;
3. Then add μL Tween 80, mix evenly;
4. Then add μL
Please ensure that the stock solution in the first step is dissolved to a clear state, and add co-solvents in sequence. You can use ultrasonic heating (ultrasonic cleaner, recommended frequency 20-40 kHz), vortexing, etc. to assist dissolution.
Protocols
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RNA extraction experimental
By lysing cells, releasing RNA, and removing impurities such as proteins and DNA, high-purity RNA products are finally obtained. The commonly used traditional method is the guanidine isothiocyanate/phenol/chloroform method (Trizol), which is suitable for a variety of animal materials including animal tissues, microorganisms, cultured cells, etc., and most plant materials.
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Apoptosis Solutions
Apoptosis is a regulated, generally non-lytic cell-death pathway that removes unwanted, damaged, infected, or abnormal cells through coordinated morphological changes, caspase activation, DNA fragmentation, and membrane remodeling. The intrinsic apoptosis pathway is controlled mainly by mitochondrial outer membrane permeabilization, BCL-2 family proteins, cytochrome c release, apoptosome formation, caspase-9 activation, and downstream executioner caspase-3/7 activation. The extrinsic apoptosis pathway is initiated by death receptors such as Fas, TNFR, and TRAIL receptors, which recruit adaptor proteins and activate caspase-8 before engaging executioner caspases or mitochondrial amplification through BID cleavage. Apoptosis is linked to many phenotypes, including cancer cell killing, tissue homeostasis, immune regulation, neurodegeneration, infection response, and treatment-induced cytotoxicity; unresolved questions include how apoptosis interacts with necroptosis, pyroptosis, ferroptos
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Research Protocol for Inflammation-related Diseases
The NLRP3 inflammasome is a cytosolic innate immune signaling platform that integrates priming signals and danger-signal activation to promote caspase-1 activation, maturation of IL-1β and IL-18, and gasdermin D-mediated pyroptotic cell death. The core experimental logic is to determine whether inflammatory disease phenotypes are driven by increased NLRP3 expression, ASC-containing inflammasome assembly, caspase-1 cleavage, GSDMD cleavage, and extracellular release of IL-1β/IL-18 rather than by nonspecific cell injury alone. The pathway is strongly linked to inflammation-related disease phenotypes because monosodium urate crystals activate NALP3/NLRP3 inflammasome signaling in gout-like crystal inflammation, cholesterol crystals activate NLRP3 inflammasomes in atherogenesis models, and DSS-induced intestinal inflammation has been reported to involve NLRP3 inflammasome activity. However, experimental colitis studies also show context-dependent protective effects of NLRP3 inflammasome co
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Pyroptosis Solutions
Pyroptosis is a lytic inflammatory cell-death pathway executed by gasdermin pores, most classically through inflammasome-mediated activation of caspase-1, cleavage of gasdermin D, membrane pore formation, LDH release, and secretion of IL-1β and IL-18. The canonical pathway is commonly modeled by priming cells with an inflammatory signal such as LPS to induce pro-IL-1β and inflammasome components, followed by an activation signal such as ATP or nigericin to activate NLRP3, ASC speck formation, caspase-1 cleavage, GSDMD cleavage, cytokine release, and pyroptotic membrane rupture. The non-canonical pathway is triggered when cytosolic LPS activates mouse caspase-11 or human caspase-4/5, leading to GSDMD cleavage and pyroptosis, and this can secondarily activate NLRP3-dependent IL-1β release. Pyroptosis is linked to inflammatory injury, infection, cancer, liver disease, ocular disease, placental inflammation, and other disease phenotypes, but unresolved questions include which gasdermin fam
Purity & Documentation
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Data Sheet (284 KB)
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SDS (396 KB)
- English - EN (396 KB)
- Français - FR (396 KB)
- Deutsch - DE (396 KB)
- Norwegian - NO (396 KB)
- Español - ES (396 KB)
- Swedish - SV (396 KB)
- Italian - IT (396 KB)
- Korean - KR (396 KB)
- Portuguese - PT (396 KB)
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Handling Instructions (2659 KB)
References
[1]. Sirianni A C, et al. N‐acetyl‐l‐tryptophan, but not N‐acetyl‐d‐tryptophan, rescues neuronal cell death in models of amyotrophic lateral sclerosis[J]. Journal of Neurochemistry, 2015, 134(5): 956-968. [Content Brief]
[2]. Li H, et al. Inhibition of excessive mitophagy by N-acetyl-L-tryptophan confers hepatoprotection against Ischemia-Reperfusion injury in rats[J]. PeerJ, 2020, 8: e8665. [Content Brief]
[3]. Thornton E, et al. The NK1 receptor antagonist N-acetyl-L-tryptophan reduces dyskinesia in a hemi-parkinsonian rodent model[J]. Parkinsonism & related disorders, 2014, 20(5): 508-513. [Content Brief]
[4]. Fernandes J, et al. N-acetyl-L-tryptophan, a substance-P receptor antagonist attenuates aluminum-induced spatial memory deficit in rats[J]. Toxicology Mechanisms and Methods, 2018, 28(5): 328-334. [Content Brief]
Complete Stock Solution Preparation Table
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
| Optional Solvent | Concentration Solvent Mass | 1 mg | 5 mg | 10 mg | 25 mg |
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| DMSO | 1 mM | 4.0607 mL | 20.3037 mL | 40.6075 mL | 101.5187 mL |
| 5 mM | 0.8121 mL | 4.0607 mL | 8.1215 mL | 20.3037 mL | |
| 10 mM | 0.4061 mL | 2.0304 mL | 4.0607 mL | 10.1519 mL | |
| 15 mM | 0.2707 mL | 1.3536 mL | 2.7072 mL | 6.7679 mL | |
| 20 mM | 0.2030 mL | 1.0152 mL | 2.0304 mL | 5.0759 mL | |
| 25 mM | 0.1624 mL | 0.8121 mL | 1.6243 mL | 4.0607 mL | |
| 30 mM | 0.1354 mL | 0.6768 mL | 1.3536 mL | 3.3840 mL | |
| 40 mM | 0.1015 mL | 0.5076 mL | 1.0152 mL | 2.5380 mL | |
| 50 mM | 0.0812 mL | 0.4061 mL | 0.8121 mL | 2.0304 mL | |
| 60 mM | 0.0677 mL | 0.3384 mL | 0.6768 mL | 1.6920 mL | |
| 80 mM | 0.0508 mL | 0.2538 mL | 0.5076 mL | 1.2690 mL | |
| 100 mM | 0.0406 mL | 0.2030 mL | 0.4061 mL | 1.0152 mL |
N-Acetyl-L-tryptophan Related Classifications
HY-W011978 Related Classifications
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