Disease relevance of NSC 57541

• Forty-one patients with chronic liver disease were sensitized with 0.1% diphenylcyclopropenone while on the waiting list for orthotopic liver transplantation [1].
• In contrast, contact hypersensitivity to diphenylcyclopropenone was significantly suppressed after ultraviolet B exposure, as was natural killer cell activity [2].
• Topical diphencyprone for alopecia areata: evaluation of 48 cases after 30 months' follow-up [3].
• Volunteers (n = 46) were randomly assigned to received no sensitization, sensitization with the allergen diphenylcyclopropenone (DPCP) on non-UV-exposed normal skin, or sensitization with DPCP on skin exposed to three minimal erythema doses (MED) of either UVA or UVB radiation 3 days before sensitization [4].
• Urticaria as a side-effect of diphencyprone therapy for resistant viral warts [5].

High impact information on NSC 57541

• Topical immunotherapy with DCP, which induced expression of HLA-DR in epidermal keratinocytes in 6 out of 13 cases, reduced the abnormal expression of both HLA-ABC and -DR antigens in the epithelium of lower hair follicles in AA [6].
• The chronic contact dermatitis was induced with daily application of diphenylcyclopropenone (DCP) on a hind paw of HDC (+/+) and HDC (-/-) mice for 2 months [7].
• Expression of vascular endothelial growth factor, apoptosis inhibitors (survivin and p16) and CCL27 in alopecia areata before and after diphencyprone treatment: an immunohistochemical study [8].
• Topical immunotherapy, using a potent contact allergen such as diphencyprone (DPC), is currently considered the most effective mode of treatment [8].
• Restoration of hair growth with topical diphencyprone in mouse and rat models of alopecia areata [9].

Chemical compound and disease context of NSC 57541

• Delayed-type hypersensitivity (DTH) reactions to the experimental allergen diphenylcyclopropenone (DCP) were measured in four groups, which either trained (+) or did not train in relaxation (-) during the sensitization and/or the challenge phase [10].
• Dinitrochlorobenzene, squaric acid dibutyl ester and diphencyprone are most commonly employed in the therapy of alopecia areata and viral warts [11].
• BACKGROUND: Topical diphenylcyclopropenone (DPCP) and minoxidil have been used in the treatment of alopecia areata with variable results [12].
• Allergic and irritant contact dermatitis compared in the treatment of alopecia totalis and universalis. A comparison of the value of topical diphencyprone and tretinoin gel [13].
• To assess the adaptation induced by solar simulated radiation, we measured the proliferative response and cytokine production of skin-draining lymph node cells after immunization to DPCP, the contact hypersensitivity (CHS) response to PCl, and thymine-thymine (T-T) cyclobutane dimers in the skin of mice [14].

Biological context of NSC 57541

• In the treated patients with a good response to diphencyprone, the mean T4/T8 ratio was 1:1, while in the patients with poor or no response to treatment, the ratio was 0 [15].
• The antioxidants were prepared by cyclization of pyridines and diazines with diphenylcyclopropenone followed by introduction of the O-substituent [16].

Anatomical context of NSC 57541

• Langerhans cells that express matrix metalloproteinase 9 increase in human dermis during sensitization to diphenylcyclopropenone in patients with alopecia areata [17].
• After induction of immunosuppression by SSR or by TL12 lamps, the proliferative response of draining lymph node cells after challenge with DPCP, or the CHS after challenge with PCl, showed significant suppression of the immune response [14].
• Diphenylcyclopropenone treatment of alopecia areata induces apoptosis of perifollicular lymphocytes [18].
• Besides topical contact sensitisers (eg, diphencyprone or dinitrochlorobenzene), newer agents of the imidazoquinoline family such as imiquimod and resiquimod act by inducing cytokine secretion from monocytes or macrophages (interferon-alpha, interleukin-12, tumour-necrosis factor-alpha) [19].
• Expression of calcium binding proteins, calretinin and calbindin-D28K, normally widely seen in dorsal horn interneurons, was up-regulated on the DCP-treated side [20].

Associations of NSC 57541 with other chemical compounds

• Although it appears somewhat less effective than published reports of dinitrochlorobenzene contact immunotherapy, diphenylcyclopropenone contact immunotherapy is an effective treatment for resistant warts and avoids any potential problems from mutagenicity [21].
• Reduced lipopolysaccharide-triggered cytokine production (of IL-12p40, IFN-gamma, IL-6 and TNF-alpha) by draining lymph node cells of mice sensitized and challenged with DPCP indicated that no adaptation is induced [14].
• The patients were subdivided into different groups depending on hair loss area, sex, pathogenesis, response to topical immune modulators (squaric acid dibutylester and diphencyprone) and age of onset of the disease [22].
• For recalcitrant common warts possible options include inosine pranobex with cryotherapy or electrosurgery, imiquimod with paring and occlusion, intralesional bleomycin, or diphencyprone [23].
• The purpose of the study was to evaluate the clinical manifestations and compare the effects of treatment with intralesional injection of triamcinolone acetonide suspension and immunotherapy with dinitrochlorobenzene (DNCB) or diphenylcyclopropenone (DPCP) [24].

Gene context of NSC 57541

• Moreover, our results suggest that TNF-alpha, which is markedly increased under DCP treatment, might be an effector of the therapeutic response in AA [25].
• E-Cadherin and alpha-N-catenin, synapse-related molecules, were intensely expressed in the spinal dorsal horn of the DCP-treated side [20].
• Vitiligo complicating diphencyprone sensitization therapy for alopecia universalis [26].
• RESULTS: Topical exposure to LF 2 h prior to sensitization caused a significant reduction in contact allergen (diphenylcyclopropenone, DPC)-induced LC migration from the epidermis as judged by the altered frequency of cells expressing either HLA-DR or CD1a determinants [27].
• Fexofenadine, an H1-receptor antagonist, partially but rapidly inhibits the itch of contact dermatitis induced by diphenylcyclopropenone in patients with alopecia areata [28].

Analytical, diagnostic and therapeutic context of NSC 57541

• In addition, a localized moderate sunburn appeared to modulate immunization with diphenylcyclopropenone through a distant, unirradiated site (41% weak responses) as compared to the control group (9%) (P = 0.05) [29].
• We concluded that patients who do not respond to diphenylcyclopropenone sensitization before transplantation develop at most mild acute rejection and that skin test scores identify patients with troublesome rejection [1].
• Topical immunotherapy with diphenylcyclopropenone (DCP) is at present the most effective approach [30].
• We investigated the solvation of several room temperature ionic liquids by Raman spectroscopy using diphenylcyclopropenone (DPCP) and phenol blue (PB) as probe molecules [31].
• By means of microsurgical lymph cannulation human skin lymph derived from the late phase of an elicitation reaction to diphenylcyclopropenone was sampled [32].

References