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Detail of "1904-98-9"

  • MSDS Download
  • CAS Number:
  • 1904-98-9
  • Name:
  • 2,6-Diaminopurine

  • Molecular Structure:
  • Formula:
  • C5H6N6
  • Molecular Weight:
  • 150.14
  • Deleted CAS:
  • 1006-52-6|39001-24-6
  • Synonyms:
  • Purine, 2, 6-diamino-;1H-Purine-2,6-diamine;SQ 21065;Purine, 2,6-diamino-;Purine, 2,6-diamino- (VAN 8CI);2-Aminoadenine;X 79;5H-purine-2,6-diamine;2,6-Dichloropurine;purine-2,6-diyldiamine;2,6-Diaminopurine 98%;9H-purine-2,6-diamine;2,6-diamino-purin;
  • EINECS:
  • 217-605-2
  • Density:
  • 1.743 g/cm3
  • Melting Point:
  • 117-122 °C(lit.)
  • Boiling Point:
  • 748.992 °C at 760 mmHg
  • Flash Point:
  • 447.815 °C
  • Solubility:
  • water: 2.38 g/L (20 °C)
  • Appearance:
  • white to light yellow crystal powder
  • Hazard Symbols:
  • HarmfulXn
  • Risk Codes:
  • 22-36/37/38-40-20/21/22
  • Safety:
  • 26-45-36/37-36/37/39-27-36-22 Details
  • particular:
  • particular

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Reference

Mitochondrial mutagenesis by 2-6-diaminopurine in Saccharomyces cerevisiae: effect of UV light
Mitochondrial mutagenesis by 2-6-diaminopurine in Saccharomyces cerevisiae: effect of UV light. Wallis, C.; Wilkie, D. (Dep. Bot. Microbiol., Univ. Coll. London, London, Engl.). Res. Photobiol., [Proc. Int. Congr.], 7th, Meeting Date 1976, 699-707. Edited by: Castellani, Amleto. Plenum: New York, N. Y. (English) 1977. CODEN: 38PEAG. DOCUMENT TYPE: Conference CA Section: 3 (Biochemical Interactions) 2,6-Diaminopurine (I) [1904-98-9] treatment of S. cerevisiae induced mitochondrial mutations resulting in increased resistance to chloramphenicol and oligomycin, decreased nos. of erythromycin-resistant mutants, and an increased incidence of petite mutants. Addnl. treatment with UV light had a synergistic effect on the induction of petite mutants. I also decreased mitochondrial protein synthesis, resulting in an absence of formation of cytochromes aa3 and b in the presence of I. I is an analog of adenine, and apparently acts by being incorporated into nucleic acid. Although the yeast mitochondria were sensitive to I, nuclei were not.
Comparative effects of adenine analogs on metabolic cooperation between Chinese hamster cells with different levels of adenine phosphoribosyltransferase activity
Comparative effects of adenine analogs on metabolic cooperation between Chinese hamster cells with different levels of adenine phosphoribosyltransferase activity. Dickerman, Lois H.; Tischfield, Jay A. (Dep. Biol., Case Western Reserve Univ., Cleveland, Ohio, USA). Mutat. Res., 49(1), 83-94 (English) 1978. CODEN: MUREAV. ISSN: 0027-5107. DOCUMENT TYPE: Journal CA Section: 3 (Biochemical Interactions) Colony formation by variant Chinese hamster cells highly resistant to adenine analogs and deficient in adenine phosphoribosyltransferase (APRT) [9027-80-9] activity was measured after cocultivation with APRT+, CHO-K1 cells in medium contg. 1 of 3 different adenine analogs. Depending on the d. of APRT+ cells and the specific adenine analog, large differences in the recovery of APRT- colonies were obsd. The particular adenine analog and APRT+ cell d. were more significant factors in the recovery of APRT- colonies than the concn. of the analog or the level of APRT activity. The no. of wild-type cells (CHO-K1) required to inhibit formation of APRT- colonies by 50% (mean lethal d.; MLD50) with 65 mg/mL 8-azaadenine [1123-54-2] as the selective drug was 1.5 ′ 104/cm2. With 100 mg/mL 2,6-diaminopurine (I) [1904-98-9] the MLD50 for CHO-K1 was 7.3 ′ 103/cm2. The MLD50 for CHO-K1 when the I concn. was decreased to 50 mg/mL was only slightly higher, 9.1 ′ 103/cm2. The most toxic effect was obsd. with 2-fluoroadenine (II) [700-49-2]. The MLD50 for CHO-K1 in 2 mg/mL II was 8.2 ′ 102/cm2, a cell d. which permits min. direct contact between APRT+ and APRT- cells. The toxic effects of II on individually resistant, APRT- cells were mediated by metabolites released into the medium by dying APRT+ cells. This metabolite toxicity to APRT- cells was also demonstrated in mixts. with cells having only 8% of wild-type APRT activity. The parameters of metabolic cooperation with individual selective agents should apparently be established before attempting to detn. mutation frequencies for mammalian cells in culture.
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