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Ditiocarb sodium (Sodium diethyldithiocarbamate) Sale

(Synonyms: 二乙基二硫代氨基甲酸钠; Sodium diethyldithiocarbamate) 目录号 : GC32142

Ditiocarb sodium (Sodium diethyldithiocarbamate) (Sodium diethyldithiocarbamate) 是铜胶结率的促进剂。

Ditiocarb sodium (Sodium diethyldithiocarbamate) Chemical Structure

Cas No.:148-18-5

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产品描述

Ditiocarb sodium (Sodium diethyldithiocarbamate) is an accelerator of the rate of copper cementation. Sodium diethyldithiocarbamate reduces the incidence of HIV infection.

Ditiocarb sodium (Sodium diethyldithiocarbamate) reacts with the Cu2+ solution giving a complex of copper diethyldithiocarbamate, which enhances the rate of cementation[1]. Ditiocarb sodium is an agent with strong antioxidant capacity and chelating activities[2].

Ditiocarb sodium (Sodium diethyldithiocarbamate) improves the depressed immune responses of newborn and aged mice. Sodium diethyldithiocarbamate prevents cisplatin nephrotoxicity in animals without reducing the antitumor activity. In that AIDS model, Ditiocarb sodium reduces lymphadenopathy and hypergammaglobulinemia, restores immunocompetence, and prolongs survival[2].

[1]. Abeer A.El-Saharty, et al. Sodium diethyldithiocarbamate as accelerator of the rate of copper cementation. The Egyptian Journal of Aquatic Research. 2015 Dec, Volume 41(4):289-293. [2]. Hersh EM, et al. Ditiocarb sodium (diethyldithiocarbamate) therapy in patients with symptomatic HIV infection and AIDS. A randomized, double-blind, placebo-controlled, multicenter study. JAMA. 1991 Mar 27;265(12):1538-44.

Chemical Properties

Cas No. 148-18-5 SDF
别名 二乙基二硫代氨基甲酸钠; Sodium diethyldithiocarbamate
Canonical SMILES [S-]C(N(CC)CC)=S.[Na+]
分子式 C5H10NNaS2 分子量 171.26
溶解度 DMSO : ≥ 300 mg/mL (1751.72 mM) 储存条件 Store at -20°C
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1 mM 5.8391 mL 29.1954 mL 58.3908 mL
5 mM 1.1678 mL 5.8391 mL 11.6782 mL
10 mM 0.5839 mL 2.9195 mL 5.8391 mL
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Research Update

Ditiocarb sodium (diethyldithiocarbamate) therapy in patients with symptomatic HIV infection and AIDS. A randomized, double-blind, placebo-controlled, multicenter study

JAMA 1991 Mar 27;265(12):1538-44.PMID:1671884doi

We randomized 389 symptomatic patients with human immunodeficiency virus (HIV) infection to Ditiocarb sodium (400 mg/m2 orally for 24 weeks) or a placebo. Patients were well balanced according to Centers for Disease Control (CDC) group, CD4+ cell number, and duration of disease prior to entry. Ten new acquired immunodeficiency syndrome (AIDS)-defining opportunistic infections occurred in the treated patients and 21 in the controls. Reduction of new opportunistic infections in the ditiocarb group was significant in all patients (relative risk [RR], 0.44) and in patients with AIDS (CDC groups IV-C1 and IV-D) (RR, 0.12). The size of the effect of ditiocarb was maintained when data were reanalyzed after exclusion of a patient who progressed to Pneumocystis carinii pneumonia who was not strictly CDC-defined (RR, 0.46), or when considering as new opportunistic infections three events, which were clinically active at entry, but for which the definitive diagnosis was made during study (RR, 0.49). The administration of ditiocarb did not induce any major adverse clinical or biological reactions. We conclude that, in this study, ditiocarb was safe and reduced the incidence of opportunistic infections in patients with symptomatic HIV infection.

Diethyldithiocarbamate (Ditiocarb sodium) effect on arachidonic acid metabolism in human mononuclear cells. Glutathione peroxidase-like activity

Biochem Pharmacol 1992 Mar 17;43(6):1319-29.PMID:1314059DOI:10.1016/0006-2952(92)90509-h.

Diethyldithiocarbamate (DTC), a thiol delivery agent, has been shown to significantly reduce the frequency of primary opportunistic infections in HIV-infected patients. This therapeutic effect has been related to the capacity of DTC to reverse the deleterious effects of the oxidative stress occurring in HIV infection. The influence of DTC on the oxygenated metabolism of arachidonic acid (AA) was investigated in mitogen-stimulated human peripheral blood mononuclear cells (PBMC). Upon incubation with PBMC previously labelled with [3H]AA, Concanavalin A (Con A) markedly increased cyclooxygenase and lipoxygenase activities, within 30 min, as judged by thromboxane B2 (TxB2) and hydroxyeicosatetraenoic acid (HETE) production. Con A activation of [3H]AA platelets also increased 12-HETE production but did not induce any TxB2 synthesis. Micromolar concentrations of DTC, added simultaneously with the mitogen, significantly enhanced the synthesis of HETEs above the Con A-induced level while TxB2-induced synthesis was inhibited but only at DTC concentrations higher than 50 microM. In the presence of nordihydroguaiaretic acid, a lipoxygenase inhibitor, which inhibited the Con A-induced synthesis of HETEs by 78%, DTC no longer stimulated HETE production above the Con A-induced level. Reverse phase HPLC analysis showed that Con A increased the PBMC production of 5-, 12- and 15-HETEs. In the presence of 5 microM DTC, 5-HETE production was entirely suppressed whereas the 15-HETE level was markedly enhanced, 12-HETE production by the contaminating platelets remained unchanged. In vitro experiments indicated that DTC alone did not significantly influence 15-hydroperoxyeicosatetraenoic (15-HPETE) production by the soybean 15-lipoxygenase but, in the presence of added reduced glutathione, DTC markedly reduced 15-HPETE into 15-HETE. In addition, DTC was able to substitute for cellular extract in the glutathione peroxidase (GPx) assay system. Taken together, these results indicate that DTC, through its "GPx-like" activity is able to modify the lipoxygenase cascade. Its ability to selectively reduce 15-HPETE known to stimulate immunosuppressive T-cells might help to explain its positive regulatory effect upon the immune system.

Randomised, double-blind, placebo-controlled trial of Ditiocarb sodium ('Imuthiol') in human immunodeficiency virus infection

Lancet 1988 Sep 24;2(8613):702-6.PMID:2901566DOI:10.1016/s0140-6736(88)90184-5.

83 patients with human immunodeficiency virus (HIV) infection (CDC groups II, III, or IV-A) were randomised in a crossover trial of sodium-diethyldithiocarbamate (Ditiocarb sodium, 'Imuthiol') (10 mg/kg body weight given orally once a week) against placebo. Each arm of the trial lasted 16 weeks. The disease did not progress to CDC-defined acquired immunodeficiency syndrome in the ditiocarb group but did so in 4 patients in the placebo group (3 between week 0 and 16, 1 between week 17 and 32). Ditiocarb was also associated to a significantly greater extent than placebo with relief of constitutional symptoms, improvement in clinical status (including shrinkage of enlarged spleen and lymph nodes), and improvement in immune function (as measured by CD4+ cell count and skin test reactivity). When placebo was replaced by ditiocarb, similar improvements were observed, whereas symptoms slowly reappeared and CD4+ cell levels progressively declined when ditiocarb treatment was replaced by placebo.

Sodium diethyldithiocarbamate (imuthiol) and cancer

Adv Exp Med Biol 1983;166:223-39.PMID:6316766DOI:10.1007/978-1-4757-1410-4_19.

Sodium diethyldithiocarbamate (imuthiol), a nonantigenic, nontoxic and noncarcinogenic compound, evinces distinctive properties in recruitment and activation of T cells, and no direct influences on B cells or macrophages. The biological attributes of imuthiol (destruction of neoplastic cells, bacteria, fungi and parasites; a detoxifying influence against carcinogens or agents toxic for the liver) could strengthen its activity as a biological response modifier. Preliminary clinic testings show that imuthiol restores T cell activities and regulates the ratio among T cell subsets in cancer patients, without untoward side effects.

Assay of Ditiocarb sodium and its methyl ester in mouse plasma by column-switching HPLC

Zhongguo Yao Li Xue Bao 1996 Sep;17(5):451-4.PMID:9863173doi

Aim: To establish a column-switching high pressure liquid chromatograpy (CSHPLC) with direct injection for determination of Ditiocarb sodium (DTC) and its methyl ester (DTC-Me) in mouse plasma. Methods: After automated online pretreating column enrichment and clear-up, DTC-Me was flushed and chromatographed on an ordinary reversed-phase analytical column, and monitored by UV at lambda absorption = 276 nm. DTC was methylated before determination. Results: No potential interfering peaks were identified. The calibration curves of both analytes were linear within the range of 0.1-150 mg.L-1. The correlation coefficients of DTC and DTC-Me were 0.9998 and 0.9995, respectively. The detection limit was 25 micrograms.L-1 and the coefficient of variation in the assay was within 7% for both compounds. The average recoveries were in the range of 95.28 -100.06%. A typical application was presented for mouse after i.v. DTC 50 mg.kg-1. Conclusion: The rapid CSHPLC method with direct injection can be used for the study of pharmacokinetics of DTC and DTC-Me.