5545-17-5

Basic information

• Product Name: (AC-CYS-OH)2
• Synonyms: 3,3'-Dithiobis[(R)-2-acetylaminopropionic acid];NSC 203780;L-Cystine, N,N'-diacetyl-;Acetylcysteine EP IMpurity C;(Ac-L-Cys-OH)2;(Ac-L-Cys-OH)2(Disulfide bond)≥ 99.5% (GC, Chiral purity);N,N'-DIACETYL-L-CYSTINE;N-ACETYL CYSTINE
• CAS NO: 5545-17-5
• Molecular Formula: C₁₀H₁₆N₂O₆S₂
• Molecular Weight: 324.37
• EINECS: 226-911-5
• Product Categories: Pharmaceuticals;Amino Acids & Derivatives;Intermediates & Fine Chemicals
• Mol File: 5545-17-5.mol
• Article Data: 41

Chemical Properties

• Melting Point: 55-72°C
• Boiling Point: 715.5 °C at 760 mmHg
• Flash Point: 386.5 °C
• Appearance: White Powder
• Density: 1.451 g/cm³
• Vapor Pressure: 2.13E-22mmHg at 25°C
• Refractive Index: 1.582
• Storage Temp.: -15°C
• Solubility: Methanol (Slightly), Water (Slightly)
• Stability: Moisture Sensitive
• CAS DataBase Reference: (AC-CYS-OH)2(CAS DataBase Reference)
• NIST Chemistry Reference: (AC-CYS-OH)2(5545-17-5)
• EPA Substance Registry System: (AC-CYS-OH)2(5545-17-5)

Safety Data

• Hazardous Substances Data: 5545-17-5(Hazardous Substances Data)

Usage

Chemical Properties

White Powder

Uses

Different sources of media describe the Uses of 5545-17-5 differently. You can refer to the following data:
1. A treatment for dermal imflammations caused by leukotriene production. Contains N-acetyl cysteine.
2. (AC-CYS-OH)2 is a disulfide dimer of N-acetylcysteine with immunomodulatory properties. Its intact disulfide bridge has been shown to be important for its ability to modify contact sensitivity/delayed hypersensitivity reactions in mice. At 3 μM/kg/day, DiNAC also demonstrates anti-atherosclerotic effects, improving endothelial function in Watanabe heritable hyperlipidemic rabbits.
3. N,N’-Diacetyl-L-cystine (DiNAC) is a disulfide dimer of N-acetylcysteine with immunomodulatory properties. Its intact disulfide bridge has been shown to be important for its ability to modify contact sensitivity/delayed hypersensitivity reactions in mice.1,2 At 3 μM/kg/day, DiNAC also demonstrates anti-atherosclerotic effects, improving endothelial function in Watanabe heritable hyperlipidemic rabbits. Acetylcysteine EP Impurity C.

InChI:InChI=1/C10H16N2O6S2/c1-5(13)11-7(9(15)16)3-19-20-4-8(10(17)18)12-6(2)14/h7-8H,3-4H2,1-2H3,(H,11,13)(H,12,14)(H,15,16)(H,17,18)/t7-,8-/m0/s1

Synthetic route

N-acetylcystein (616-91-1) → N,N'-diacetyl-L-cystine (5545-17-5)

Conditions	Yield
With bis(4-methoxyphenyl)telluride; 5,15,10,20-tetraphenylporphyrin In dichloromethane; isopropyl alcohol at 0℃; for 0.25h; Irradiation;	100%
With (bis(2,1-phenylene)bis(azanediyl)bis(methylene)diphenol)diselenide In water; acetonitrile at 20℃; for 7h;	83%
With (+)-flavinophane Fl(7) In methanol; water at 30℃; Rate constant; pH 9.55; other (+)- and (-)-flavinophanes and 5-deazaflavinophanes; asymmetric discrimination;

L-Cysteine (52-90-4) + acetic anhydride (108-24-7) → N,N'-diacetyl-L-cystine (5545-17-5)

Conditions	Yield
With sodium hydroxide for 0.5h; Ambient temperature;	22%

N,N'-diacetyl-L-cystine dimethyl ester (32381-28-5) → N,N'-diacetyl-L-cystine (5545-17-5)

Conditions	Yield
durch Verseifung;

N,N'-diacetyl-L-cystine dipropyl ester (1033249-05-6) → N,N'-diacetyl-L-cystine (5545-17-5)

Conditions	Yield
durch Verseifung;

L-cystine (56-89-3) + acetic anhydride (108-24-7) → N,N'-diacetyl-L-cystine (5545-17-5)

Conditions	Yield
With sodium hydroxide
With potassium hydroxide

N-acetylcystein (616-91-1) → N,N'-diacetyl-L-cystine (5545-17-5) + S-nitroso-N-acetylcysteine (56577-02-7)

Conditions	Yield
With hydrogenchloride; sodium nitrite at 25℃;	A n/a B 82 % Chromat.

N-acetylcystein (616-91-1) → N,N'-diacetyl-L-cystine (5545-17-5) + (R)-2-Acetylamino-3-((R)-2-acetylamino-2-carboxy-ethylsulfanyl)-propionic acid

Conditions	Yield
With water Quantum yield; Mechanism; γ-radiation (radiolysis); also with NaN3;

N-acetylcystein (616-91-1) + S-nitroso-N-acetylcysteine (56577-02-7) → N,N'-diacetyl-L-cystine (5545-17-5)

Conditions	Yield
In water at 25℃; Rate constant; also in the presence of var. conc. of EDTA;

N.N'-diacetyl-DL-cystine → N,N'-diacetyl-L-cystine (5545-17-5)

Conditions	Yield
With brucine durch Zerlegung;

S-nitroso-N-acetylcysteine (56577-02-7) → N,N'-diacetyl-L-cystine (5545-17-5)

Conditions	Yield
In water at 25℃; for 19.6667h; Quantum yield; Kinetics; Further Variations:; Solvents; also in the dark; Dimerization; UV-irradiation;
With ethylenediaminetetraacetic acid; hydroxide In water Kinetics; Further Variations:; pH dependence; Radiolysis;
With sodium hydrogen sulfide In water Acidic conditions;
With Cu2O

N-acetylcystein (616-91-1) + trans,trans,trans-[PtCl2(OH)2(c-C6H11NH2)(NH3)] (124721-03-5, 1313200-52-0, 146924-11-0) → N,N'-diacetyl-L-cystine (5545-17-5) + trans-[Pt(OH)2(c-C6H11NH2)(NH3)] (1034767-14-0)

Conditions	Yield
In water Kinetics; react. with N-acetyl-L-cysteine at pH 9 at 25°C;

dopamine (51-61-6) + N-acetylcystein (616-91-1) → N,N'-diacetyl-L-cystine (5545-17-5) + 2-S-(N-acetyl)-cysteinyl-dopamine + 5-S-(N-acetyl)-cysteinyl-dopamine + 2-S-5-S-di-(N-acetyl)-cysteinyl-dopamine

Conditions	Yield
Stage #1: dopamine With dihydrogen peroxide; lactoperoxidase at 25℃; pH=7.5; aq. phosphate buffer; Enzymatic reaction; Stage #2: N-acetylcystein at 20℃; for 0.166667h; pH=7.5; aq. phosphate buffer;

N-acetylcystein (616-91-1) → N,N'-diacetyl-L-cystine (5545-17-5) + C4H9NO2*BrH

Conditions	Yield
With C(13)C4H8AuBr2(15)NO2S2 In dimethylsulfoxide-d6 for 4h;

(R)-2-[3,5-Bis-((R)-1-carboxy-2-mercapto-ethylcarbamoyl)-benzoylamino]-3-mercapto-propionic acid (858675-87-3) + N-acetylcystein (616-91-1) + (2S,2'S)-N1,N1’-(1,3-phenylene)bis(2-(2-mercaptoacetamido)succinamide) (1597415-37-6) → N,N'-diacetyl-L-cystine (5545-17-5) + C28H38N8O12S4 + C33H42N6O18S6 + C41H48N10O18S6

Conditions	Yield
In dimethyl sulfoxide at 20℃; for 24h; pH=6.5;

ethanol (64-17-5) + N,N'-diacetyl-L-cystine (5545-17-5) → N,N'-diacetyl-L-cystine diethyl ester (24037-21-6)

Conditions	Yield
With sulfuric acid

N,N'-diacetyl-L-cystine (5545-17-5) + potassium cyanide (151-50-8) → (4R)-3-acetyl-2-imino-thiazolidine-4-carboxylic acid (142582-26-1)

Conditions	Yield
With water anschliessend mit wss. H2O2 behandeln;

N,N'-diacetyl-L-cystine (5545-17-5) → L-cystine (56-89-3)

Conditions	Yield
With n-HCl

N,N'-diacetyl-L-cystine (5545-17-5) → N,N'-diacetyl-DL-cystine (5545-17-5, 97247-12-6, 139602-29-2)

Conditions	Yield
With acetic anhydride; acetic acid at 27℃; entsteht Gemisch von racem. und meso-N.N'-Diacetyl-cystin;

diazomethane (186581-53-3, 908094-01-9) + N,N'-diacetyl-L-cystine (5545-17-5) → N,N'-diacetyl-L-cystine dimethyl ester (32381-28-5)

Conditions	Yield
In methanol; diethyl ether

N,N'-diacetyl-L-cystine (5545-17-5) + methylamine (74-89-5) → N,N'-diacetyl-L-cystine bismethylamide (13028-62-1)

Conditions	Yield
(i) CH2N2, Et2O, (ii) ClCO2Et, N-methylmorpholine, THF, (iii) /BRN= 741851/, H2O; Multistep reaction;

N,N'-diacetyl-L-cystine (5545-17-5) → N-acetyl-S-bromo-L-cysteine

Conditions	Yield
With bromine In dichloromethane; acetic acid at 0℃;

N,N'-diacetyl-L-cystine (5545-17-5) + enzyme-substance from rats liver → ammonia (7664-41-7)

N,N'-diacetyl-L-cystine (5545-17-5) → cysteine disulfide (56-89-3, 349-46-2, 923-32-0, 6020-39-9, 24645-67-8, 35100-73-3, 40143-67-7)

Conditions	Yield
Multi-step reaction with 2 steps 1: n-HCl 2: hydrochloric acid View Scheme
Multi-step reaction with 2 steps 1: n-HCl 2: hydrochloric acid View Scheme

N,N'-diacetyl-L-cystine (5545-17-5) → L-cystine (6020-39-9)

Conditions	Yield
Multi-step reaction with 2 steps 1: n-HCl 2: hydrochloric acid View Scheme

N,N'-diacetyl-L-cystine (5545-17-5) → DL-cystine (923-32-0)

Conditions	Yield
Multi-step reaction with 2 steps 1: n-HCl 2: hydrochloric acid View Scheme

N,N'-diacetyl-L-cystine (5545-17-5) → (R)-N-[2-mercapto-1-(3-methyl-1,2,4-oxadiazol-5-yl)-ethyl]-acetamide

Upstream product

• 7218-04-4 N-Acetylcysteine 
• 454-29-5 2-amino-4-mercaptobutyric acid 
• 152305-87-8 sulfosuccinimidyl acetate 
• 616-91-1 N-acetylcystein 
• 119-26-6 (2,4-dinitro-phenyl)-hydrazine 
• 32381-28-5 N,N'-diacetyl-L-cystine dimethyl ester 
• 1033249-05-6 N,N'-diacetyl-L-cystine dipropyl ester 
• 56-89-3 L-cystine 
• 108-24-7 acetic anhydride 
• 52-90-4 L-Cysteine 
• 56577-02-7 S-nitroso-N-acetylcysteine 
• 124721-03-5 trans,trans,trans-[PtCl₂(OH)2(c-C₆H₁₁NH₂)(NH₃)] 
• 51-61-6 dopamine 
• 858675-87-3 (R)-2-[3,5-Bis-((R)-1-carboxy-2-mercapto-ethylcarbamoyl)-benzoylamino]-3-mercapto-propionic acid 

Downstream Products

• 142582-26-1 (4R)-3-acetyl-2-imino-thiazolidine-4-carboxylic acid 
• 56-89-3 L-cystine 
• 5545-17-5 N,N'-diacetyl-DL-cystine 
• 56-89-3 cysteine disulfide 
• 6020-39-9 L-cystine 
• 923-32-0 DL-cystine 
• 55585-92-7 N-acetyl-homocysteine 

Relevant articles and documents

On N-acetylcysteine. Part I. Experimental and theoretical approaches of the N-acetylcysteine/H2O2 complexation

The complexation of N-acetylcysteine (RSH) with hydrogen peroxide has been studied experimentally and theoretically. Experimentally we have measured the evolution of RSH, H2O2, and RSSR (N-acetylcystine) as a function of time. Surprisingly, H2O2 decays by a biphasic process, which is not the case for RSH and RSSR. In the first stage of the kinetics, H2O2 disappears without oxidizing the thiol function of RSH. By analogy with glutathione (GSH), the formation of a complex between RSH and H2O2 has been proposed. The thermodynamic equilibrium constant of complex formation has been determined. Theoretical calculations were performed within the SIBFA method to pinpoint the sites of complexation in isolated and hydrated states. A mixed 'discrete-continuum' model was used to evaluate the solvent effect. The two stable complexes found in isolated state have different behaviour under the influence of the solvent. Comparison with complexed GSH is discussed.

Entropy-Controlled Cu(II)-Catalyzed Oxidation of N-Acetyl-L-Cysteine by Methylene Blue in Acidic Medium

Kinetics of the oxidation of N-acetyl-L-cysteine (NAC) by methylene blue (MB) catalyzed by Cu(II) have been investigated in presence of HCl. The reaction follows a first order kinetics in MB while the concentration order in NAC is zero. Hydrogen ions retard the rate of reaction. The reaction involves the participation of nanoparticles as revealed by SEM, XRD and FTIR techniques and a gel-like Cu-NAC network acts like the effective catalyst. The reaction conforms to Eley-Rideal mechanism at lower [NAC] while at higher [NAC], the kinetics are explained by extended Eley-Rideal mechanism. The reaction is regulated by the size and morphology of the nanoparticles and is controlled by the entropy of activation.

Enhanced Cellular Polysulfides Negatively Regulate TLR4 Signaling and Mitigate Lethal Endotoxin Shock

Cysteine persulfide and cysteine polysulfides are cysteine derivatives having sulfane sulfur atoms bound to cysteine thiol. Accumulating evidence has suggested that cysteine persulfides/polysulfides are abundant in prokaryotes and eukaryotes and play important roles in diverse biological processes such as antioxidant host defense and redox-dependent signal transduction. Here, we show that enhancement of cellular polysulfides by using polysulfide donors developed in this study resulted in marked inhibition of lipopolysaccharide (LPS)-initiated macrophage activation. Polysulfide donor treatment strongly suppressed LPS-induced pro-inflammatory responses in macrophages by inhibiting Toll-like receptor 4 (TLR4) signaling. Other TLR signaling stimulants—including zymosan A-TLR2 and poly(I:C)-TLR3—were also significantly suppressed by polysulfur donor treatment. Administration of polysulfide donors protected mice from lethal endotoxin shock. These data indicate that cellular polysulfides negatively regulate TLR4-mediated pro-inflammatory signaling and hence constitute a potential target for inflammatory disorders. Zhang et al. developed potent persulfide donors consisting of sulfane sulfur atoms stabilized by N-acetyl-L-cysteine (NAC polysulfides) via disulfide bonds at both sides. Strong anti-inflammatory activity of NAC polysulfides was demonstrated in cultured macrophage models and a mouse endotoxin shock model.

On N-acetylcysteine. Part II. Oxidation of N-acetylcysteine by hydrogen peroxide: Kinetic study of the overall process

The oxidation kinetics of N-acetylcysteine (RSH) by hydrogen peroxide has been studied at neutral pH at different concentration ratios from 0.2 to 20 (4 x 10-4 mol L-1 ≤ [RSH]0 ≤ 2 x 10- mol L-1, 10-4 mol L-1 ≤ [H2O2]0 ≤ 10-2 mol L-1). In all the cases studied, N-acetyleystine (RSSR) is the only oxidized product formed. Our kinetic data have focused on the importance of the concentration ratio to reach the stoichiometric oxidation of N-acetylcysteine by hydrogen peroxide. Indeed non-stoichiometric oxidation of RSH occurs at relatively low concentration ratios (R 2.5. Moreover, it has been shown that in the first minutes of the reaction there is the formation of a complex between RSH and H2O2, the stoichiometry of the complex being RSH concentration-dependent for a given R (R > 2.5). Reaction mechanisms have been quantitatively established and the k values of each step determined.

PROCESS OF MAKING N,N'-DIACETYL-L-CYSTINE

An effective process of making Ν,Ν'-diacetyl-L-Cystine ( NDAC ), which process is fast, green, does not require labor-intensive isolation or purification of the product, by yielding products in desired ratio, and has improved yield and purity. The process comprising the steps of Forming a reaction mixture, starting with a cystine derivative di-tert- butyl-L-cystine as the dihydrochloride form; Acetylating said di-tert-butyl-L-cystine to obtain Ν,Ν'-diacetyl-di-tert- butyl-L-cystine; followed by Removing said tert- butyl groups from said Ν,Ν'-diacetyl-di-tert-butyl- L-cystine to obtain Ν,Ν'-diacetyl-L-cystine product; and Isolating said Ν,Ν'-diacetyl-L-Cystine product from said reaction mixture; wherein said acetylating agent is acetic anhydride.

Thiol-based michael-type addition. A systematic evaluation of its controlling factors

This paper is about the factors controlling kinetics and product stability of this popular bioconjugation reaction. We demonstrate that a) thiol pKa, i.e. the amount of thiolates, is the only determinant of the reaction kinetics for the nucleophile; b) product degradation occurs primarily via hydrolysis (not thiol exchange), and is more prominent for the most rapidly reacting electrophiles. In terms of molecular design, acrylamides and low pKa thiols appear as the reaction partners that provide the best compromise for stability and reaction rate.