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Two new p-terphenyls, strepantibins A and B (1 and 2), along with the first representative of a naturally occurring bisphenyltropone, strepantibin C (3), were characterized from a Streptomyces sp. associated with the larvae of the mud dauber wasp Sceliphron madraspatanum. Their structures were determined by high-resolution electrospray ionization mass spectrometry, NMR, and X-ray crystallography data interpretation. Strepantibins A-C inhibited hexokinase II (HK2) activity and displayed antiproliferative activity against hepatoma carcinoma cells HepG-2, SMMC-7721 and plc-prf-5. In SMMC-7721 cells treated with strepantibin A, the morphological characteristics of apoptosis were observed.

Four angucycline glycosides were previously characterized from marine-derived Streptomyces sp. OC1610.4. Further investigation of this strain cultured on different fermentation media from that used previously resulted in the isolation of two new angucycline glycosides, vineomycins E and F ( 1 - 2 ), and five known homologues, grincamycin L ( 3 ), vineomycinone B 2 ( 4 ), fridamycin D ( 5 ), moromycin B ( 7 ), and saquayamycin B 1 ( 8 ). Vineomycin F ( 2 ) contains an unusual ring-cleavage deoxy sugar. All the angucycline glycosides isolated from Streptomyces sp. OC1610.4 were evaluated for their cytotoxic activity against breast cancer cells MCF-7, MDA-MB-231, and BT-474. Moromycin B ( 7 ), saquayamycin B 1 ( 8 ), and saquayamycin B ( 9 ) displayed potent anti-proliferation against the tested cell lines, with IC 50 values ranging from 0.16 to 0.67 μM. Saquayamycin B ( 9 ) inhibited the migration and invasion of MDA-MB-231 cells in a dose-dependent manner, as detected by Transwell and wound-healing assays.

Background & Objective: Chronic myeloid leukemia (CML) in blast phase is refractory with a poor prognosis. This study was to evaluate efficacy of imatinib mesylate, a specific inhibitor of BCR/ABL tyrosine kinase, on CML in blast phase., Methods: Nineteen patients with CML in blast phase (imatinib treatment group) received induction of cytarabine-based standard chemotherapy for 2 cycles, and 400 mg/d of imatinib mesylate for 4 weeks. Patients with no remission received 600 mg/d of imatinib mesylate for another 8 weeks. Treatment of 600 mg/d of imatinib mesylate was maintained if it showed effects after 8 weeks, otherwise it would be stopped. Twenty-two patients with CML in blast phase (historical control group) received inducement of cytarabine-based chemotherapy for 2 cycles, and other regimens of consolidation or continuous induction., Results: Sixteen patients of imatinib treatment group achieved no hematologic remission after induction. After treated with imatinib mesylate, 6 of 16 (38%) achieved hematologic complete remission (CHR), and major cytogenetic response; 2 of 16(13%) achieved hematologic partial remission (PHR); 1 of 16 (6%) returned to chronic phase with minor cytogenetic response. Total hematologic response rate of imatinib treatment group was 57%; 1-year survival rate was 38% (6/16). Eighteen patients of historical control group achieved no hematologic remission after inducement. After treated with other regimens, 2 (11%) achieved CHR, and 1 (6%) achieved PHR. Total hematologic response rate of historical control group was 17%; 1-year survival rate was 6%(1/18), significantly lower than that of imatinib treatment group (P< 0.05)., Conclusions: Imatinib mesylate may have anti-leukemic activity, and prolong survival time of patients with CML in blast phase. But problems of tumor relapse, and drug resistance are still present.