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Chemical Compound Review

NSC-82344     oxo-dipropan-2-yloxy- phosphanium

Synonyms: AC1O3FKK, NSC82344, ZINC02577585, LS-106576, NSC 82344, ...
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Disease relevance of DFP

  • Afferent granuloma cells produced a plasminogen-dependent, DFP inhibitable protease activity that was dependent on the cell concentration and the incubation time [1].
  • When soman or DFP was administered subcutaneously in high doses a severe AChE inhibition was obtained in iris without any concomitant miosis [2].
  • Motor incoordination (rotarod test) produced by DFP exposure had a rapid onset, with complete recovery by 10 hr [3].
  • Further administration of DFP (0.5 mg/kg/day, sc) for 6-14 days led to tolerance development as evidenced by disappearance of the described toxicity signs [4].
  • Further administration of DFP (14 days) caused disappearance of fasciculations and loss of sensitivity to the necrotizing actions in all muscles tested (diaphragm, soleus, and extensor digitorum longus) [5].

Psychiatry related information on DFP


High impact information on DFP

  • Enzymatic activity of cathepsin G is associated with its monocyte chemotactic activity, since DFP- or PMSF-inactivated cathepsin G no longer induced monocyte migration [8].
  • Recovery of PA activity from neutrophils was critically dependent on pretreatment of the intact cells with DFP before cavitation; 100-fold more PA activity was detected in DFP-pretreated cells [9].
  • Serine proteases or esterases released from cell cultures into the growth medium were converted to radioactive derivatives by active site labeling with tritiated DFP, both in the presence and absence of other competing active site reagents [10].
  • Other ligands (free uPA, ATF and DFP-treated uPA) were not internalized nor degraded [11].
  • Compared with control subjects, both diabetic and nondiabetic twins showed greater LPS-induced downregulation of monocyte COX-1 mRNA (P = 0.02), reduced upregulation of COX-2 mRNA and protein (P < 0.03), and greater inhibition by the COX-2 inhibitor di-isopropylfluorophosphate (DFP) of monocyte PGE(2) (P < 0.007) [12].

Chemical compound and disease context of DFP


Biological context of DFP

  • Poorly or non-phosphorylating analogues of the cyclohexyl alkylphosphonofluoridates of DFP were not inhibitory; nor did fluoride, the hydrolysis product of these inhibitors, inhibit ingestion under either condition [17].
  • Both the enzymatic and hemolytic activity of D were irreversibly inhibited by treatment with 10 mM DFP as well as by reduction and alkylation [18].
  • In contrast to tissue thromboplastin produced by other M phi populations, the H-M phi PCA was found to be markedly sensitive both to heat inactivation at 56 degrees C and to inhibition by 1 mM DFP [19].
  • The inhibitors of methyltransferase, SIBA, adenosine, or HEH showed a dose-dependent inhibitory effect not only on phospholipid methylation but also on serine esterase activation and on BCDF-induced IgG production; DFP inhibited IgG production but not phospholipid methylation [20].
  • In synchronized cells, signals provided by TRF could be transduced only when cells were in the G1-phase, and DFP showed an inhibitory effect only when it was added to cells in the G1-phase with TRF [21].

Anatomical context of DFP

  • All three antibodies partially inhibited the binding of EAC14o23b to tonsil lymphocytes and, in the presence of 0.1 mM DFP, to Raji cells; binding of EAC14o23bi and EAC14o23d to tonsil cells was not affected [22].
  • In order to isolate the DFP binding peptide, liver microsomes were labeled with [3H]DFP and the 60-kDa protein containing covalently bound DFP isolated in pure form [23].
  • Expression of the mutagenized cDNAs in COS-1 cells demonstrated that any single substitution of Gly629, Ser631, or Gly633 with other residues resulted in the complete loss of the enzyme activity and DFP binding [24].
  • The alteration in NF subunit protein levels observed in DFP-treated hen spinal cords was not observed in protected hens [25].
  • In 36-day-old chicks, PMSF (300 mg/kg) promoted OPIDP when given up to 5 days after DFP (1.5 mg/kg) when residual NTE inhibition in brain and sciatic nerve was about 40% [26].

Associations of DFP with other chemical compounds


Gene context of DFP

  • 4. No changes in any CSF release or HT-29 cell apoptosis were detected in the presence of the COX-2 selective inhibitor DFP (10(-7)-10(-4) M) [31].
  • The enzyme activity was inhibited by serine-protease inhibitors, such as DFP and PMSF, indicating that the KEX2 endopeptidase belongs to a serine-protease family [32].
  • Hence the DFP induced astroglial pathology as indicated by the complex expression profile of GFAP and vimentin mRNA levels may be playing an important role in the delayed degeneration of axons or is the result of progressive degeneration of axons in OPIDN [33].
  • At 1 1/2 and 24 hr after the DFP treatments, BuChE was considerably more depressed than was the case for AChE [34].
  • Plasma from indomethacin- or DFP-, but not from SC-560-treated rats abolished cyclooxygenase-2 activity in activated A549 cells [35].

Analytical, diagnostic and therapeutic context of DFP

  • Following reduction and carboxymethylation, the DFP-labeled protein was fragmented with trypsin and the digest subjected to gel filtration [23].
  • Two young adult cats were given a single, intraperitoneal injection of di-isopropylfluorophosphate (DFP) [36].
  • Young adult cats were given a single intraperitoneal injection of di-isopropylfluorophosphate (DFP) and were killed 14, 18, 20, 21, and 28 days later by intracardiac perfusion with aldehydes [37].
  • The Flinders Sensitive Line (FSL) rat, selectively bred for increased responses to the anticholinesterase DFP, was originally proposed as an animal model of depression because, like depressed humans, it is supersensitive to the behavioral and hormonal effects of cholinergic (muscarinic) agonists [38].
  • The results indicate that effective prosthetic orifice area may be computed by the pressure independent equation A = 21SV/DFP2, where A is the effective prosthesis orifice area in cm2, SV is the stroke volume in ml and DFP is the diastolic filling period in s min-1 [39].


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