Kanki Komiyama

Structure of cypemycin, a new peptide antibiotic

Abstract The structure of cypemycin, a new peptide antibiotic, was determined by means of FAB-MS, NMR, and amino acid analysis. The data have revealed cypemycin as being a structurally unique peptide antibiotic that contains a sulfide bridge at its C-terminus as well as four α,β-unsaturated amino acids.

Structures of novel antibiotics, furaquinocins A and B

Structures of novel citocydal antibiotics furaquinocins A and B, isolated from the fermentation broth of Streptomyces sp. KO-3988, was elucidated on the basis of spectroscopic analyses.

Structure of phenazinomycin, a novel antitumor antibiotic

Abstract Structure and absolute configuration of a novel antitumor antibiotic phenazinomycin was determined on the basis of the spectral data and chemical degradation. Phenazinomycin is the first phenazinone alkaloid which possesses sesquiterpene moiety in its structure.

Leucophyllidine, a Cytotoxic Bisindole Alkaloid Constituted From the Union of an Eburnan and a New Vinylquinoline Alkaloid

A cytotoxic bisindole alkaloid possessing an unprecedented structure constituted from the union of an eburnan half and a novel vinylquinoline alkaloid has been isolated from Leuconotis griffithii. The structure was established by analysis of the spectroscopic data and confirmed by X-ray diffraction analysis. A possible biogenetic pathway to the novel quinolinic coupling partner is presented from an Aspidosperma precursor.

Angustilobine and andranginine type indole alkaloids and an uleine-secovallesamine bisindole alkaloid from Alstonia angustiloba.

A total of 20 alkaloids were isolated from the leaf and stem-bark extracts of Alstonia angustiloba, of which two are hitherto unknown. One is an alkaloid of the angustilobine type (angustilobine C), while the other is a bisindole alkaloid angustiphylline, derived from the union of uleine and secovallesamine moieties. The structures of these alkaloids were established using NMR and MS analysis. Angustilobine C showed moderate cytotoxicity towards KB cells.

Aspidospermatan-aspidospermatan and eburnane-sarpagine bisindole alkaloids from Leuconotis

Leucofoline and leuconoline, representing the first members of the aspidospermatan-aspidospermatan and eburnane-sarpagine subclasses of the bisindole alkaloids, respectively, were isolated from the Malayan Leuconotis griffithii. The structures of these bisindole alkaloids were established using NMR and MS analysis, and in the case of leuconoline, confirmed by X-ray diffraction analysis. Both alkaloids showed weak cytotoxicity towards human KB cells.

CCDC 755717: Experimental Crystal Structure Determination

Related Article: Chew-Yan Gan, W.T.Robinson, T.Etoh, M.Hayashi, K.Komiyama, Toh-Seok Kam|2009|Org.Lett.|11|3962|doi:10.1021/ol9016172

Histopathological studies on antitumor effect of sporamycin

SummaryMice that had received transplants of sarcoma-180 followed by treatment with sporamycin were examined histopathologically at periodic intervals. A marked degeneration of tumor cells was observed at an early stage after the administration of sporamycin, but the degeneration subsequently ceased and regrowth of the tumor was seen. Marked infiltration of lymphoid cells, granulation tissue, and fibrosis was seen in the stroma or surrounding tissue of the tumor at a late stage after the administration of sporamycin, and the regression of tumor cells became marked. With a few exceptions the mice were completely cured by about the 40th day.In the peripheral lymphoid tissues, a transitory decrease in the number of cells was observed after the administration of sporamycin, but this was followed by regeneration of the cells, followed by a marked increase in the B cell system. On the other hand, lymphoid cell depletion of the thymus had persisted.Transplantation of intact sarcoma-180 to mice preliminarily inoculated with sporamycin-treated sarcoma-180 cells resulted in inhibition of tumor growth in most of the mice, and qualitatively the same tissue reactions as those in mice cured of sarcoma-180 by sporamycin were seen.The results suggest that enhancement both of antigenicity of the tumor (cells) and of the subsequent immune response of the host by sporamycin may be involved in the cure of the experimental tumor.

Mechanism of action of acetyl kidamycin. I. Interaction with DNA.

Acetyl kidamycin, an antitumor antibiotic, was strongly bound to DNA in vitro, consequently, the melting temperature of DNA was significantly increased, and its buoyant density was decreased. From these results, it was suggested that acetyl kidamycin stabilized residual links between complementary strands by binding to DNA. An additional action was observed in that acetyl kidamycin caused single-strand scission of DNA in an alkaline sucrose density gradient solution.

Effect of antitumor agents on sarcoma-180 tumor cells transplanted to liver, kidney, and lung.

The survival time of animals, inhibition of the incorporation of thymidine-[6-3H] (3H-TdR) into DNA, and histopathological observation were made after the injection of Mitomycin-C, Bleomycin, cyclophosphamide, Daunomycin, Actinomycin-D, or 5-fluorouracil into mice transplanted with sarcoma-180 to their liver, kidney, and lung. The most prolonged survival time was obtained by the injection with cyclophosphamide and a moderate prolonged survival by Bleomycin and Actinomycin-D. In the case of 5-fluorouracil and Daunomycin, there were extreme variations in the survival time depending on the site of tumor growth. Cyclophosphamide and 5-fluorouracil showed greater and longer lasting inhibition of the incorporation of 3H-TdR into DNA of the tumor tissue, whereas the remaining agents caused transient inhibition on the tumor tissue. Inhibitory ratio and duration of the incorporation of 3H-TdR into DNA of normal site of the tissue of tumor-bearing organ were found to be more increased or almost the same compared with those of the tumor tissue. The most rapid recovery of the incorporation of 3H-TdR into DNA was observed in the small intestine among various organs and tumor in any treatment groups. From the histopathological observation, the degree of tumor cell damage by the agent was almost in agreement with inhibition of the incorporation of 3H-TdR up to 72 hr after the treatment.