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Phosphoramide mustard is a chemical compound that serves as a cytotoxin or cell-killing agent, primarily used in chemotherapy medications like cyclophosphamide. It is characterized by the presence of two amine groups and is responsible for the cytotoxic activity of cyclophosphamide by forming covalent bonds with DNA in cancer cells, thereby inhibiting cell division and causing cell death. Metabolized in the liver, phosphoramide mustard is associated with harmful side effects such as immunosuppression and potential carcinogenesis, necessitating careful handling in medical and scientific contexts.

10159-53-2

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10159-53-2 Usage

Uses

Used in Oncology:
Phosphoramide mustard is used as a cytotoxic agent for the treatment of various cancers. It is metabolized from cyclophosphamide in the liver and plays a crucial role in the chemotherapeutic process by inhibiting the division of cancer cells and inducing cell death.
Used in Drug Metabolism:
Phosphoramide mustard is used as a metabolic product in the liver, where it is formed from cyclophosphamide. This conversion is essential for the drug's cytotoxic activity, as it is the active form that interacts with DNA in cancer cells.
Used in Medical Research:
Phosphoramide mustard is used as a subject of study in medical research to understand its cytotoxic effects, side effects, and potential applications in cancer treatment. Researchers aim to minimize its harmful effects and improve its therapeutic efficacy.
Used in Drug Safety and Handling:
Phosphoramide mustard is used as a reference compound in the development of safety protocols and handling guidelines for medical and scientific professionals. Due to its potential carcinogenic and immunosuppressive effects, it is crucial to minimize exposure and ensure proper handling to protect the health of those working with it.

Check Digit Verification of cas no

The CAS Registry Mumber 10159-53-2 includes 8 digits separated into 3 groups by hyphens. The first part of the number,starting from the left, has 5 digits, 1,0,1,5 and 9 respectively; the second part has 2 digits, 5 and 3 respectively.
Calculate Digit Verification of CAS Registry Number 10159-53:
(7*1)+(6*0)+(5*1)+(4*5)+(3*9)+(2*5)+(1*3)=72
72 % 10 = 2
So 10159-53-2 is a valid CAS Registry Number.
InChI:InChI=1/C4H11Cl2N2O2P/c5-1-3-8(4-2-6)11(7,9)10/h1-4H2,(H3,7,9,10)

10159-53-2SDS

SAFETY DATA SHEETS

According to Globally Harmonized System of Classification and Labelling of Chemicals (GHS) - Sixth revised edition

Version: 1.0

Creation Date: Aug 10, 2017

Revision Date: Aug 10, 2017

1.Identification

1.1 GHS Product identifier

Product name phosphoramide mustard

1.2 Other means of identification

Product number -
Other names Phosphamide mustard

1.3 Recommended use of the chemical and restrictions on use

Identified uses For industry use only.
Uses advised against no data available

1.4 Supplier's details

1.5 Emergency phone number

Emergency phone number -
Service hours Monday to Friday, 9am-5pm (Standard time zone: UTC/GMT +8 hours).

More Details:10159-53-2 SDS

10159-53-2Related news

phosphoramide mustard (cas 10159-53-2) induces autophagy markers and mTOR inhibition prevents follicle loss due to phosphoramide mustard (cas 10159-53-2) exposure07/18/2019

Phosphoramide mustard (PM) is an ovotoxic metabolite of cyclophosphamide. Postnatal day 4 Fisher 344 rat ovaries were exposed to vehicle control (1% DMSO) or PM (60 μM) ± LY294002 or rapamycin for 2 or 4 d. Transmission election microscopy revealed abnormally large golgi apparatus and electron...detailed

10159-53-2Relevant academic research and scientific papers

The partitioning of phosphoramide mustard and its aziridinium ions among alkylation and P-N bond hydrolysis reactions

Shulman-Roskes, Ellen M.,Noe, Dennis A.,Gamcsik, Michael P.,Marlow, Allison L.,Hilton, John,Hausheer, Frederick H.,Colvin, O. Michael,Ludeman, Susan M.

, p. 515 - 529 (1998)

NMR (1H and 31P) and HPLC techniques were used to study the partitioning of phosphoramide mustard (PM) and its aziridinium ions among alkylation and P-N bond hydrolysis reactions as a function of the concentration and strength of added nucleophiles at 37 °C and pH 7.4. With water as the nucleophile, bisalkylation accounted for only 10-13% of the product distribution given by PM. The remainder of the products resulted from P-N bond hydrolysis reactions. With 50 mM thiosulfate or 55-110 mM glutathione (GSH), bisalkylation by a strong nucleophile increased to 55- 76%. The rest of the PM was lost to either HOH alkylation or P-N bond hydrolysis reactions. Strong experimental and theoretical evidence was obtained to support the hypothesis that the P-N bond scission observed at neutral pH does not occur in the parent PM to produce nornitrogen mustard; rather it is an aziridinium ion derived from PM which undergoes P-N bond hydrolysis to give chloroethylaziridine. In every buffer studied (bis-Tris, lutidine, triethanolamine, and Tris), the decomposition of PM (with and without GSH) gave rise to 31P NMR signals which could not be attributed to products of HOH or GSH alkylation or P-N bond hydrolysis. The intensities of these unidentified signals were dependent on the concentration of buffer.

Design, synthesis and evaluation of targeted hypoxia-activated prodrugs applied to chondrosarcoma chemotherapy

Canitrot, Damien,Chezal, Jean-Michel,Galmier, Marie-Josephe,Gaumet, Vincent,Gerard, Yvain,Ghedira, Donia,Maubert, Elise,Miot-Noirault, Elisabeth,Peyrode, Caroline,Tarrit, Sebastien,Voissière, Aurélien,Weber, Valérie

, (2020)

The tumor microenvironment in chondrosarcoma (CHS), a chemo- and radio-resistant cancer provides unique hallmarks for developing a chondrosarcoma targeted drug‐delivery system. Tumor targeting could be achieved using a quaternary ammonium function (QA) as a ligand for aggrecan, the main high negative charged proteoglycan of the extracellular matrix of CHS, and a 2-nitroimidazole as trigger that enables hypoxia‐responsive drug release. In a previous work, ICF05016 was identified as efficient proteoglycan-targeting hypoxia-activated prodrug in a human extraskeletal myxoid chondrosarcoma model in mice and a first study of the structure-activity relationship of the QA function and the alkyl linker length was conducted. Here, we report the second part of the study, namely the modification of the nitro-aromatic trigger and the position of the proteoglycan-targeting ligand at the aromatic ring as well as the nature of the alkylating mustard. Synthetic approaches have been established to functionalize the 2-nitroimidazole ring at the N-1 and C-4 positions with a terminal tertiary alkyl amine, and to perform the phosphorylation step namely through the use of an amine borane complex, leading to phosphoramide and isophosphoramide mustards and also to a phosphoramide mustard bearing four 2-chloroethyl chains. In a preliminary study using a reductive chemical activation, QA-conjugates, except the 4-nitrobenzyl one, were showed to undergo efficient cleavage with release of the corresponding mustard. However N,N,N-trimethylpropylaminium tethered to the N-1 or C-4 positions of the imidazole seemed to hamper the enzymatic reduction of the prodrugs and all tested compounds featured moderate selectivity toward hypoxic cells, likely not sufficient for application as hypoxia-activated prodrugs.

Improving nature's enzyme active site with genetically encoded unnatural amino acids

Jackson, Jennifer C.,Duffy, Sean P.,Hess, Kenneth R.,Mehl, Ryan A.

, p. 11124 - 11127 (2006)

The ability to site-specifically incorporate a diverse set of unnatural amino acids (>30) into proteins and quickly add new structures of interest has recently changed our approach to protein use and study. One important question yet unaddressed with unnatural amino acids (UAAs) is whether they can improve the activity of an enzyme beyond that available from the natural 20 amino acids. Herein, we report the >30-fold improvement of prodrug activator nitroreductase activity with an UAA over that of the native active site and a >2.3-fold improvement over the best possible natural amino acid. Because immense structural and electrostatic diversity at a single location can be sampled very quickly, UAAs can be implemented to improve enzyme active sites and tune a site to multiple substrates.

Nitrobenzyl-based photosensitive phosphoramide mustards: Synthesis and photochemical properties of potential prodrugs for cancer therapy

Reinhard, Robert,Schmidt, Brigitte F.

, p. 2434 - 2441 (2007/10/03)

Several nitrobenzyl-based photosensitive phosphoramide mustards were synthesized. The nitrobenzyl moiety was structurally varied to find the most promising prodrug candidates in respect to photorelease and activity of the alkylating species. The synthesis of these compounds proved to be applicable even in regard to compounds with additional functionalization. The target molecules 13a,b to 14 exhibited the expected red shift in their absorption spectra maximum compared to the parent nitrobenzyl moiety. As seen by UV and 31P NMR spectroscopy, the phosphoramide mustard was quickly liberated upon irradiation with mercury arc lamps. Assaying the structurally different prodrugs on their alkylating activity showed that compounds 13b and 14, derived from secondary benzyl alcohols, are promising prodrug candidates. Their water solubility and the possibility of attaching macromolecules are encouraging vis-a-vis future investigations on their in vitro cytotoxicity.

Synthesis, Activation, and Cytotoxicity of Aldophosphamide Analogues

Borch, Richard F.,Valente, Ronald R.

, p. 3052 - 3058 (2007/10/02)

A series of perhydrooxazine analogues of aldophosphamide has been prepared, and their 31P NMR kinetics and in vitro cytotoxicity have been evaluated.These compounds were developed on the basis of the idea that ring opening and tautomerization to an enamine intermediate might provide a mechanistic alternative to the β-elimination reaction for release of phosphoramide mustard.The 4,4,6-trimethyltetrahydro-1,3-oxazine moiety was selected on the basis of its rapid rate of iminium ion generation and relatively slow rate of hydrolysis.These analogues underwent phosphorodiamidate release by three distinct mechanisms: hydrolysis to aldophosphamide and subsequent β-elimination; cyclization to produce the 4-hydroxycyclophosphamides, which release phosphorodiamidate by ring opening and elimination; and tautomerization to the enamine with rapid expulsion of phosphorodiamidate.Kinetic studies demonstrated that hydrolysis to the aldehyde contributed minimally to the overall activation process and that the enamine pathway represented the major route of activation.For those analogues that could undergo cyclization this pathway competed effectively with enamine release, and these analogues were essentially equivalent to their 4-hydroxycyclophosphamide counterparts in cytotoxicity.A series of tetra-N-substituted phosphorodiamidates that cannot undergo cyclization was prepared to explore the effects of cyclization on the cytotoxicity of these analogues.The tetrakis(chloroethyl)phosphorodiamidates were highly potent in vitro against both cyclophosphamide-sensitive and -resistant L1210 and P388 cell lines, and one of these analogues had significant antitumor activity against L1210 leukemia in vivo.These results demonstrate that the enamine mechanism provides a viable pathway for delivery of phosphorodiamidates and that this approach can be used to deliver phosphorodiamidates that are non-cross-resistant in cyclophosphamide-resistant cell lines.

Aldophosphamide Acetal Diacetate and Structural Analogues: Synthesis and Cytotoxicity Studies

Wang, Yuqiang,Farquhar, David

, p. 197 - 203 (2007/10/02)

The synthesis of aldophosphamide acetal diacetate and a number of structural analogues is described.These compounds are designed to undergo biotransformation to the corresponding aldehydes in the presence of carboxylate esterases, enzymes that are ubiquitous in mammalian tissue.Several of these aldehydes can theoretically exist in pseudoequilibrium with the 4-hydroxyoxazaphosphorine tautomers; others lack this capability.The half-lives of the acetals in 0.05 M phosphate buffer, pH 7.4, at 37 deg C ranged from 1 to 2 days.In the presence of 2 unit equiv of porcine liver carboxylate esterase, all of the compounds were hydrolyzed with half-lives of less than 1 min.Although closely structurally related, the compounds exhibited a wide range of cytotoxicities to L1210 murine leukemia cells in vitro.

NMR Spectroscopic Studies of Intermediary Metabolites of Cyclophosphamide. A Comprehensive Kinetic Analysis of the Interconversion of cis- and trans-4-Hydroxycyclophosphamide with Aldophosphamide and the Concomitant Partitioning of Aldophosphamide between Irreversible Fragmentation ...

Zon, Gerald,Ludeman, Susan Marie,Brandt, Joan A.,Boyd, Victoria L.,Oezkan, Gunay,et al.

, p. 466 - 485 (2007/10/02)

Multinuclear (31P, 13C, 2H, and 1H) Fourier-transform NMR spectroscopy, with and without isotopically enriched materials, was used to identify and quantify, as a function of time, the following intermediary (short-lived) metabolites of the anticancer prodrug cyclophosphamide (1, Scheme I): cis-4-hydroxycyclophosphamide (cis-2), its trans isomer (trans-2), aldophosphamide (3), and its aldehyde-hydrate (5).Under a standard set of reaction conditions (1 M 2,6-dimethylpyridine buffer, pH 7.4, 37 deg C), the stereospecific deoxygenation of synthetic cis-4-hydroperoxycyclophosphamide (cis-12, 20 mM) with 4 equiv of sodium thiosulfate (Na2S2O3) afforded, after ca.20 min, a "pseudoequilibrium" distribution of cis-2, 3, 5, and trans-2, i.e., the relative proportions of these reactants (57:4:9:30, respectively) remained constant during their continual disappearance.NMR absorption signals indicative of "iminophosphamide" (8) and enol 6 were not detected ( "3" trans-2, as well as the rate constant (k3) for the irreversible fragmentation of 3.The values of k3 at pH 6.3, 7.4, and 7.8 were equal to 0.030 +/- 0.004, 0.090 +/- 0.008, and 0.169 +/- 0.006 min-1, respectively.Replacement of the HC(O)CH2 moiety in 3 with HC(O)CD2 led to a primary kinetic isotope effect (kH/kD = 5.6 +/- 0.4) for k3.The apparent half-lives (τ*1/2) for cis-2, "3", and trans-2 under the standard reaction conditions, at "pseudoequilibrium" (constant ratio of cis-2/"3"/trans-2), were each equal to ca.38 min, which is considerably shorter than the widely cited colorimetrically derived half-lives reported by earlier investigators.The values of τ*1/2 for cis-2, "3", and trans-2 were affected by pH in the same manner as that found for k3 but were relatively insensitive to the presence of either K(+), Na(+), Ca(2+), or Mg(2+).The presence of certain primary amines led to marked decreases in τ*1/2 and, in some cases, the formation of acyclic adducts of aldehyde 3.The relatively stable adduct formed from 3 and tris(hydroxymethyl)aminomethane (Tris) at pH 7.4 and 37 deg C gave rise to a 31P NMR signal that other investigators have mistakenly ascribed to 2. 31P NMR spectroscopy was also used to examine, in considerable detail, the manifold effects of N-acetyl-L-cysteine upon the chemistry of 2, "3", and 4, which featured the formation of a mixture of diastereomeric, acyclic ...

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