이소니아지드

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• 그림문자(GHS)

  

• 신호 어

  Warning

• 유해·위험 문구

  H302：삼키면 유해함

  H315：피부에 자극을 일으킴

• 예방조치문구

  P264：취급 후에는 손을 철저히 씻으시오.

  P264：취급 후에는 손을 철저히 씻으시오.

  P270：이 제품을 사용할 때에는 먹거나, 마시거나 흡연하지 마시오.

  P280：보호장갑/보호의/보안경/안면보호구를 착용하시오.

  P301+P312：삼켜서 불편함을 느끼면 의료기관(의사)의 진찰을 받으시오.

  P302+P352：피부에 묻으면 다량의 물로 씻으시오.

  P332+P313：피부 자극이 생기면 의학적인 조치· 조언을 구하시오.

이소니아지드 MSDS

• INAH

이소니아지드 화학적 특성, 용도, 생산

• 물성

  Isoniazid는 프로 드럭입니다. 그것은 박테리아 카탈라아제에 의해 활성화되어야합니다. 활성화 된 Isoniazid는 미 콜린 산 합성을 방지합니다. Mycolic acids는 중요한 박테리아 세포벽 성분입니다. 치료 수준에서, Isoniazid는 활발히 성장하는 세포 내 및 세포 외 결핵균 유기체 에 대한 박테리오 제형입니다 . 특히, Isoniazid는 NAD 보조 인자와 공유 결합 부가 물을 만들어 InhA에 영향을 줄 것이다.

• 개요

  이소니아지드(Laniazid, Nydrazid, isonicotinylhydrazine, INH)는 1차 항결핵제로서 예방과 치료에 쓰이는 유기화합물이다. 1912년 처음으로 발견되었으며, 1951년에 결핵에 대하여 효과적임을 알게 되었다. 이소니아지드는 활동적인 결핵에 단독으로 쓰이지 않는데, 이는 내성이 쉽게 생기기 때문이다. 이소니아지드는 또한 항우울제의 효과가 있으며, 이른 시기에 발견된 항우울제이기도 하다.

• 용도

  Isoniazid는 일종의 항 박테리아 물질로 주로 결핵성 물질로 사용됩니다. 지금까지 Isoniazide는 여전히 결핵 치료를위한 선택입니다. Isoniazid는 Mycobacterium 속의 미생물, 특히 M. tuberculosis, M. bovis 및 M. kansasii 와 싸울 때 유용합니다. Isoniazid는 매우 특수한 제약 원료입니다. 다른 미생물에 대해서는 효과가 없습니다. 이소니아지드는 급속히 분열하는 마이코 박테리아에 대해 살균 작용을하지만, 마이코 박테리아가 서서히 자라는 경우에는 정균입니다. Isoniazid는 다른 항 결핵약과 함께 사용할 수 있습니다.

• 개요

  Isoniazid, the hydrazide of isonicotinic acid was introduced into medical practice for treating tuberculosis in 1953. Isoniazid exhibits bactericidal action on Mycobacterium tuberculosis. It inhibits the synthesis of mycolic acid, an important component of the cell membrane of mycobacteria. Mycolic acid is specific only to mycobacteria, and it is the cause of the selective toxicity of the drug with respect to these microorganisms.
  Mutants that are resistant to isoniazid are rarely seen in nature, and in a spontaneously growing population of tuberculous bacillus there is approximately one mutant in every 105 –106 organisms. Large populations of microorganisms of the order 109 –1010 bacilli in the pulmonary cavities contain a significant number of resistant mutants. If only isoniazid is taken during treatment, an increased number of mutants will be observed and they will eventually become the dominant phenotype. The transformation from sensitive to nonsensitive microorganisms during treatment is called secondary or acquired resistance, which can originate over the course of a few weeks. Isoniazid is the most important drug for treating pulmonary and nonpulmonary forms of tuberculosis. It is active against both intracellular and extracellular organisms. In order to prevent secondary resistance, isoniazid should be used with other effective drugs (usually rifampin). Synonyms of this drug are tubazid, andrazide, niazid, piridizin, and many others.

• 화학적 성질

  white crystalline powder

• 용도

  Isoniazid is an antimicrobial used for the prevention of tuberculosis infection or used concurrently with another agent for the treatment of tuberculosis infection. Rifampin, pyrazinamide, or both of these agents are commonly used with isoniazid. Isoniazid is the only Food and Drug Administration approved drug to treat latent tuberculosis in order to prevent it from becoming active.

• Indications

  Isoniazid (isonicotinic acid hydrazide, or INH) is the most active drug for the treatment of tuberculosis caused by susceptible strains. It is a synthetic agent with a structural similarity to that of pyridoxine.

• 정의

  ChEBI: A carbohydrazide obtained by formal condensation between pyridine-4-carboxylic acid and hydrazine.

• Biological Functions

  Its action is bactericidal against replicating organisms, but it appears to be only bacteriostatic at best against semidormant and dormant populations. After treatment with INH, M . tuberculosis loses its acid fastness, which may be interpreted as indicating that the drug interferes with cell wall development.

• Antimicrobial activity

  Susceptibility to isoniazid is virtually restricted to the M. tuberculosis complex (MIC 0.01–0.2 mg/L). It is highly bactericidal against actively replicating M. tuberculosis. Other mycobacteria are resistant, except for some strains of M. xenopi (MIC 0.2 mg/L) and a few strains of M. kansasii (MIC 1 mg/L).

• 원료

  Mutations in the katG gene, the inhA gene or its promoter region, and in the intergenic region of the oxyR–ahpC locus confer resistance to isoniazid. The relative proportions of such mutations vary geographically and are related to the distribution of the various lineages or superfamilies of M. tuberculosis.
  Isoniazid resistance is the commonest form of drug resistance worldwide and the great majority of strains resistant to another agent are also resistant to isoniazid.

• 일반 설명

  Odorless colorless or white crystals or white crystalline powder. Taste is slightly sweet at first and then bitter. pH (1% aqueous solution) 5.5-6.5. pH (5% aqueous solution) 6-8.

• 공기와 물의 반응

  Sensitive to air and light. Absorbs insignificant amounts of moisture at 77°F at relative humidities up to approximately 90%. Water soluble. Dust can be explosive when suspended in air at specific concentrations.

• 반응 프로필

  Isoniazid is incompatible with chloral, aldehydes, iodine, hypochlorites and ferric salts. Isoniazid is also incompatible with oxidizers. Isoniazid may react with sugars and ketones. Isoniazid can react as a weak acid or a weak base. Isoniazid can be decomposed by oxidative and reductive reactions.

• 화재위험

  Isoniazid is combustible.

• Pharmaceutical Applications

  One of a number of nicotinamide analogs found to have antituberculosis activity, following the observation that nicotinamide inhibited the replication of M. tuberculosis. It is soluble in water. The dry powder is stable if protected from light. It is a prodrug requiring oxidative activation by KatG, a mycobacterial catalase–peroxidase enzyme.

• Mechanism of action

  Isoniazid is active against susceptible bacteria only when they are undergoing cell division. Susceptible bacteria may continue to undergo one or two divisions before multiplication is arrested. Isoniazid can inhibit the synthesis of mycolic acids, which are essential components of mycobacterial cell walls.The mycobacterial enzyme catalase– peroxidase KatG activates the administered isoniazid to its biologically active form.The target sites for the activated isoniazid action are acyl carrier protein AcpM and Kas A, a β-ketoaceyl carrier protein synthetase that blocks mycolic acid synthesis. Isoniazid exerts its lethal effects at the target sites by forming covalent complexes.

• Pharmacokinetics

  Oral absorption: >95%
  C_max 300 mg oral: 3–5 mg/L after 1–2 h
  Plasma half-life: 0.5–1.5 h (rapid acetylators)
  : 2–4 h (slow acetylators)
  Volume of distribution: 0.6–0.8 L/kg
  Plasma protein binding: Very low
  Absorption and distribution
  Isoniazid is almost completely absorbed from the gut and is well distributed. Absorption is impaired by aluminum hydroxide. Therapeutic concentrations are achieved in sputum and CSF. It crosses the placenta and is found in breast milk.
  Metabolism
  Isoniazid is extensively metabolized to a variety of pharmacologically inactive derivatives, predominantly by acetylation. As a result of genetic polymorphism, patients are divisible into rapid and slow acetylators. About 50% of Caucasians and Blacks, but 80–90% of Chinese and Japanese, are rapid acetylators. Acetylation status does not affect the efficacy of daily administered therapy. The rate of acetylation is reduced in chronic renal failure.
  Excretion
  Nearly all the dose is excreted in the urine within 24 h, as unchanged drug and metabolic products.

• Pharmacology

  Isoniazid is water soluble and is well absorbed when administered either orally or parenterally. Oral absorption is decreased by concurrent administration of aluminum-containing antacids.
  Isoniazid does not bind to serum proteins; it diffuses readily into all body fluids and cells, including the caseous tuberculous lesions. The drug is detectable in significant quantities in pleural and ascitic fluids, as well as in saliva and skin. The concentrations in the central nervous system (CNS) and cerebrospinal fluid are generally about 20% of plasma levels but may reach close to 100% in the presence of meningeal inflammation.
  Isoniazid is acetylated to acetyl isoniazid by N-acetyltransferase, an enzyme in liver, bowel, and kidney. Individuals who are genetically rapid acetylators will have a higher ratio of acetyl isoniazid to isoniazid than will slow acetylators. Rapid acetylators were once thought to be more prone to hepatotoxicity, but this is not proved. The slow or rapid acetylation of isoniazid is rarely important clinically, although slow inactivators tend to develop peripheral neuropathy more readily. Metabolites of isoniazid and small amounts of unaltered drug are excreted in the urine within 24 hours of administration.

• Clinical Use

  Isonicotinic acid hydrazide, isonicotinyl hydrazide, or INH(Nydrazid) occurs as a nearly colorless crystalline solid thatis very soluble in water. It is prepared by reacting the methylester of isonicotinic acid with hydrazine.
  Isoniazid is a remarkably effective agent and continuesto be one of the primary drugs (along with rifampin, pyrazinamide,and ethambutol) for the treatment of tuberculosis.It is not, however, uniformly effective against all formsof the disease. The frequent emergence of strains of the tuberclebacillus resistant to isoniazid during therapy wasseen as the major shortcoming of the drug. This problemhas been largely, but not entirely, overcome with the use ofcombinations.
  The activity of isoniazid is manifested on the growing tuberclebacilli and not on resting forms. Its action, which isconsidered bactericidal, is to cause the bacilli to lose lipidcontent by a mechanism that has not been fully elucidated.The most generally accepted theory suggests that the principaleffect of isoniazid is to inhibit the synthesis of mycolicacids, high–molecular-weight, branched β-hydroxyfatty acids that constitute important components of the cellwalls of mycobacteria.

• 부작용

  The incidence and severity of adverse reactions to isoniazid are related to dosage and duration of therapy. Isoniazid-induced hepatitis and peripheral neuropathy are two major untoward effects.

• 환경귀착

  Isoniazid is a colorless, odorless, white crystalline powder that is slowly oxidized by exposure to air. It undergoes degradation upon prolonged exposure to light. Isoniazid has a solubility of 1 g per 8 ml water, 1 g per 50 ml ethanol, and it is slightly soluble in chloroform and very slightly soluble in ether. A 10% solution of isoniazid has a pH of 6.0–8.0.

• 신진 대사

  Isoniazid is extensively metabolized to inactive metabolites. The major metabolite is N-acetylisoniazid. The enzyme responsible for acetylation, cytosolic N-acetyltransferase, is produced under genetic control in an inherited autosomal fashion. Individuals who possess high concentrations of the enzyme are referred to as rapid acetylators, whereas those with low concentrations are slow acetylators. This may result in a need to adjust the dosage for fast acetylators. The N-acetyltransferase is located primarily in the liver and small intestine. Other metabolites include isonicotinic acid, which is found in the urine as a glycine conjugate, and hydrazine. Isonicotinic acid also may result from hydrolysis of acetylisoniazid, but in this case, the second product of hydrolysis is acetylhydrazine. Acetylhydrazine is acetylated by N-acetyltransferase to the inactive diacetyl product. This reaction occurs more rapidly in rapid acetylators. The formation of acetylhydrazine is significant in that this compound has been associated with the hepatotoxicity, which may occur during INH therapy.

• Purification Methods

  Crystallise isoniazide from 95% EtOH and dry it in a vacuum. [Beilstein 22 III/IV 545, 22/2 V 219.]

• 주의 사항

  High isoniazid plasma levels inhibit phenytoin metabolismand potentiate phenytoin toxicity when the twodrugs are coadministered. The serum concentrations ofphenytoin should be monitored, and the dose should beadjusted if necessary.

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