本研究评估了乙胺嘧啶和磺胺嘧啶在治疗急性感染期间感染多种非典型弓形虫的小鼠的疗效。总共七株弓形虫被注射到瑞士小鼠体内。受感染小鼠的治疗选择是乙胺嘧啶每天 3-200 毫克/公斤，磺胺嘧啶每天 10-640 毫克/公斤，或两种药物组合的较低剂量。为了评估基因型和对乙胺嘧啶和/或磺胺嘧啶的敏感性之间的关系，采用了描述性分析。菌株 TgCTBr4 和 TgCTBr17（基因型 108）对乙胺嘧啶或磺胺嘧啶治疗的反应较差。菌株 TgCTBr1 和 TgCTBr25（基因型 206）对 PYR 同样敏感，但对磺胺嘧啶治疗不敏感。唯一对两种药物治疗反应良好的菌株是 TgCTBr9 菌株（基因型 11）[1]。

Absorption, Distribution and Excretion
Sulfadiazine is excreted largely in the urine.
Very limited penetration through the skin. Only when applied to very large area burns is absorption into the body generally an issue.

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Metabolism / Metabolites
Sulfadiazine has known human metabolites that include Sulfadiazine hydroxylamine.

Hepatotoxicity
Sulfadiazine, like other sulfonamides, causes a characteristic idiosyncratic liver injury which has features of drug-allergy or hypersensitivity. The typical onset is sudden development of fever and rash followed by jaundice within a few days or weeks of starting the medication. The pattern of injury is typically mixed, although fatal cases are often hepatocellular and prolonged cholestatic cases have also been described. Eosinophilia or atypical lymphocytosis are also common and the clinical pattern can be considered a part of DRESS syndrome (drug rash with eosinophilia and systemic symptoms). Cases of Stevens Johnson syndrome due to sulfadiazine have also been described. Sulfonamides such as sulfadiazine have been linked to many cases of acute liver failure and as a class, the sulfonamides still rank in the top 5 to 10 causes of drug induced, idiosyncratic fulminant hepatic failure. However, most cases of sulfonamide induced liver injury resolve rapidly, usually within 2 to 4 weeks unless cholestasis is severe. Onset of injury is more rapid with rechallenge and can appear within a day or reexposure. Patients with hepatic injury due to sulfadiazine may have a history of previous exposure to the drug without injury. Sulfonamides such as sulfadiazine can also cause mild and transient ALT elevations that do not progress to jaundice or more severe liver injury either alone or as a part of a generalized hypersensitivity reaction. Sulfonamides have also been linked to hepatic granulomas.

[1]. Kopmann C, et al. Abundance and transferability of antibiotic resistance as related to the fate of sulfadiazine in maize rhizosphere and bulk soil. FEMS Microbiol Ecol. 2013 Jan;83(1):125-34.
[2]. Silva LA, et al. Efficacy of sulfadiazine and pyrimetamine for treatment of experimental toxoplasmosis with strains obtained from human cases of congenital disease in Brazil. Exp Parasitol. 2019 Jul;202:7-14.

Sulfadiazine is a sulfonamide consisting of pyrimidine with a 4-aminobenzenesulfonamido group at the 2-position. It has a role as an antimicrobial agent, an antiinfective agent, a coccidiostat, an antiprotozoal drug, an EC 2.5.1.15 (dihydropteroate synthase) inhibitor, an EC 1.1.1.153 [sepiapterin reductase (L-erythro-7,8-dihydrobiopterin forming)] inhibitor, a xenobiotic, an environmental contaminant and a drug allergen. It is a member of pyrimidines, a sulfonamide, a substituted aniline and a sulfonamide antibiotic. It is functionally related to a sulfanilamide. It is a conjugate acid of a sulfadiazinate.
Sulfadiazine is an antibacterial prescription medicine approved by the U.S. Food and Drug Administration (FDA) for the prevention and treatment of certain types of bacterial infections, including the treatment of chancroid, Toxoplasma gondii encephalitis, urinary tract infections, and other infections.
Toxoplasma gondii encephalitis can be an opportunistic infection (OI) of HIV.
One of the short-acting sulfonamides used in combination with pyrimethamine to treat toxoplasmosis in patients with acquired immunodeficiency syndrome and in newborns with congenital infections.
Silver sulfadiazine is a sulfa derivative topical antibacterial used primarily on second- and third-degree burns.
Sulfadiazine is a Sulfonamide Antibacterial.
Sulfadiazine is a sulfonamide antibacterial agent used in the therapy of mild-to-moderate infections due to sensitive organisms. Sulfadiazine, like other sulfonamides, is a well known cause of clinically apparent, idiosyncratic liver injury.
Sulfadiazine has been reported in Apis cerana with data available.
Sulfadiazine is a synthetic pyrimidinyl sulfonamide derivative, short-acting bacteriostatic Sulfadiazine inhibits bacterial folic acid synthesis by competing with para amino benzoic acid. It is used in combination with pyrimethamine to treat toxoplasmosis in patients with acquired immunodeficiency syndrome and in newborns with congenital infections. (NCI04)
Silver Sulfadiazine is a sulfonamide-based topical agent with antibacterial and antifungal activity. Silver sulfadiazine may act through a combination of the activity of silver and sulfadiazine. When this agent interacts with sodium chloride-containing body fluids, silver ions are released slowly and sustainably into wounded areas. Ionized silver atoms catalyze the formation of disulfide bonds leading to protein structural changes and inactivating thiol-containing enzymes; silver ions may also intercalate DNA thereby interfering with replication and transcription of bacteria. As a competitive inhibitor of para-aminobenzoic acid (PABA), sulfadiazine inhibits bacterial dihydropteroate synthase, thereby resulting in disruption of folic acid metabolism and ultimately DNA synthesis.
One of the short-acting SULFONAMIDES used in combination with PYRIMETHAMINE to treat toxoplasmosis in patients with acquired immunodeficiency syndrome and in newborns with congenital infections.
See also: Silver Sulfadiazine (has salt form); Sulfadiazine Sodium (has salt form); Sulfadiazine; Trimethoprim (component of) ... View More ...

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Drug Indication
For the treatment of rheumatic fever and meningococcal meningitis
Indicated as an adjunct for the prevention and treatment of wound sepsis in patients with second- and third-degree burns.

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Mechanism of Action
Sulfadiazine is a competitive inhibitor of the bacterial enzyme dihydropteroate synthetase. This enzyme is needed for the proper processing of para-aminobenzoic acid (PABA) which is essential for folic acid synthesis. The inhibited reaction is necessary in these organisms for the synthesis of folic acid.
Studies utilizing radioactive micronized silver sulfadiazine, electron microscopy, and biochemical techniques have revealed that the mechanism of action of silver sulfadiazine on bacteria differs from silver nitrate and sodium sulfadiazine. Silver sulfadiazine acts only on the cell membrane and cell wall to produce its bactericidal effect. A specific mechanism of action has not been determined, but silver sulfadiazine's effectiveness may possibly be from a synergistic interaction, or the action of each component. Silver is a biocide, which binds to a broad range of targets. Silver ions bind to nucleophilic amino acids, as well as sulfhydryl, amino, imidazole, phosphate, and carboxyl groups in proteins, causing protein denaturation and enzyme inhibition. Silver binds to surface membranes and proteins, causing proton leaks in the membrane, leading to cell death. Sulfadiazine is a competitive inhibitor of bacterial para-aminobenzoic acid (PABA), a substrate of the enzyme dihydropteroate synthetase. The inhibited reaction is necessary in these organisms for the synthesis of folic acid.

C10H10N4O2S

250.276

250.052

68-35-9

Sulfadiazine sodium;547-32-0;Sulfadiazine-d4;1020719-78-1;Sulfadiazine-13C6;1189426-16-1

5215

White to off-white solid powder

1.5±0.1 g/cm3

512.6±52.0 °C at 760 mmHg

253 °C (dec.)(lit.)

263.8±30.7 °C

0.0±1.3 mmHg at 25°C

1.679

-0.12

106.35

2

6

3

17

327

0

S(C1C([H])=C([H])C(=C([H])C=1[H])N([H])[H])(N([H])C1=NC([H])=C([H])C([H])=N1)(=O)=O

SEEPANYCNGTZFQ-UHFFFAOYSA-N

InChI=1S/C10H10N4O2S/c11-8-2-4-9(5-3-8)17(15,16)14-10-12-6-1-7-13-10/h1-7H,11H2,(H,12,13,14)

4-amino-N-pyrimidin-2-ylbenzenesulfonamide

RP 2616; RP2616; RP-2616

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO : ≥ 50 mg/mL (~199.78 mM)
H2O : < 0.1 mg/mL

配方 1 中的溶解度: ≥ 2.5 mg/mL (9.99 mM) (饱和度未知) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将100 μL 25.0 mg/mL澄清DMSO储备液加入到400 μL PEG300中，混匀；然后向上述溶液中加入50 μL Tween-80，混匀；加入450 μL生理盐水定容至1 mL。
*生理盐水的制备：将 0.9 g 氯化钠溶解在 100 mL ddH₂O中，得到澄清溶液。

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配方 2 中的溶解度: 2.5 mg/mL (9.99 mM) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (这些助溶剂从左到右依次添加，逐一添加), 悬浊液; 超声助溶。
例如，若需制备1 mL的工作液，可将 100 μL 25.0 mg/mL澄清DMSO储备液加入900 μL 20% SBE-β-CD生理盐水溶液中，混匀。
*20% SBE-β-CD 生理盐水溶液的制备（4°C，1 周）：将 2 g SBE-β-CD 溶解于 10 mL 生理盐水中，得到澄清溶液。

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配方 3 中的溶解度: ≥ 2.5 mg/mL (9.99 mM) (饱和度未知) in 10% DMSO + 90% Corn Oil (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将 100 μL 25.0 mg/mL 澄清 DMSO 储备液加入到 900 μL 玉米油中并混合均匀。

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请根据您的实验动物和给药方式选择适当的溶解配方/方案：
1、请先配制澄清的储备液(如：用DMSO配置50 或 100 mg/mL母液(储备液));
2、取适量母液，按从左到右的顺序依次添加助溶剂，澄清后再加入下一助溶剂。以 下列配方为例说明 (注意此配方只用于说明，并不一定代表此产品 的实际溶解配方):
10% DMSO → 40% PEG300 → 5% Tween-80 → 45% ddH2O (或 saline);
假设最终工作液的体积为 1 mL, 浓度为5 mg/mL: 取 100 μL 50 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀/澄清；向上述体系中加入50 μL Tween-80，混合均匀/澄清；然后继续加入450 μL ddH2O (或 saline)定容至 1 mL；
3、溶剂前显示的百分比是指该溶剂在最终溶液/工作液中的体积所占比例;
4、 如产品在配制过程中出现沉淀/析出，可通过加热(≤50℃)或超声的方式助溶;
5、为保证最佳实验结果，工作液请现配现用！
6、如不确定怎么将母液配置成体内动物实验的工作液，请查看说明书或联系我们;
7、 以上所有助溶剂都可在 Invivochem.cn网站购买。