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Lithiation of R2P(CH2C9H6N-8)NBut (R = Ph, 3; R = Pri, 4) with an equivalent of BunLi afforded lithium iminophosphorano(8-quinolyl)methanide [Li{CH(8-C9H6N)P(Ph2)NBut}(THF)] (5) and [Li{CH(8-C9H6N)P(Pri 2)NBut}]2 (6), respectively. Reaction of 4 with Et2Mg yielded magnesium iminophosphorano(8-quinolyl)methanide complex (7). Treatment of 6 with ZnCl2 gave [Zn(Cl){CH(8-C9H6N)P(Pri 2)NBut}] (8), which was transformed into alkylated zinc complexes [Zn(R1){CH(8-C9H6N)P(Pri 2)NBut}] (R1 = Ph, 9; R1 = Me, 10) by treating with R1Li or R1MgX. Ethylzinc complexes [Zn(Et){CH(8-C9H6N)P(R2)NBut}] (R = Ph, 11; R = Pri, 12) were obtained by reaction of 3 or 4 with an equivalent of Et2Zn. Compounds 2 and 4 − 12 were characterized by 1H, 13C{1H}, and 31P{1H} NMR spectroscopy and elemental analyses. Structures of complexes 6 − 8 and 10 were further characterized by single-crystal X-ray diffraction techniques. The catalytic behaviors of complexes 7 and 9 − 12 in the ring-opening polymerization of ε-caprolactone was studied. Complex 7 exhibited high catalytic activity in the presence or absence of benzyl alcohol. Complexes 9 − 12 catalyzed the ring-opening polymerization of ε-CL in the presence of benzyl alcohol and exhibited first-order dependence on monomer concentration.

A series of Al(III) and Sn(II) diiminophosphinate complexes have been synthesized. Reaction of Ph(ArCH2)P(NBut)NHBut (Ar = Ph, 3; Ar = 8‐quinolyl, 4) with AlR3 (R = Me, Et) gave aluminum complexes [R2Al{(NBut)2P(Ph)(CH2Ar)}] (R = Me, Ar = Ph, 5; R = Me, Ar = 8‐quinolyl, 6; R = Et, Ar = Ph, 7; R = Et, Ar = quinolyl, 8). Lithiated 3 and 4 were treated with SnCl2 to afford tin(II) complexes [ClSn{(NBut)2P(Ph)(CH2Ar)}] (Ar = Ph, 9; Ar = 8‐quinolyl, 10). Complex 9 was converted to [(Me3Si)2NSn{(NBut)2P(Ph)(CH2Ph)}] (11) by treatment with LiN(SiMe3)2. Complex 11 was also obtained by reaction of 3 with [Sn{N(SiMe3)2}2]. Complex 9 reacted with [LiOC6H4But‐4] to yield [4‐ButC6H4OSn{(NBut)2P(Ph)(CH2Ph)}] (12). Compounds 3–12 were characterized by NMR spectroscopy and elemental analysis. The structures of complexes 6, 10, and 11 were further characterized by single crystal X‐ray diffraction techniques. The catalytic activity of complexes 5–8, 11, and 12 toward the ring‐opening polymerization of ε‐caprolactone (CL) was studied. In the presence of BzOH, the complexes catalyzed the ring‐opening polymerization of ε‐CL in the activity order of 5 > 7 ≈ 8 > 6 ≫ 11 > 12, giving polymers with narrow molecular weight distributions. The kinetic studies showed a first‐order dependency on the monomer concentration in each case. © 2006 Wiley Periodicals, Inc. J Polym Sci Part A: Polym Chem 44: 4621–4631, 2006

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Inhibition of interleukin–6 (IL-6) holds significant promise as a therapeutic approach for triple negative breast cancer (TNBC). We previously reported that phenylmethimazole (C10) reduces IL-6 expression in several cancer cell lines. We have identified a more potent derivative of C10 termed COB-141. In the present work, we tested the hypothesis that C10 and COB-141 inhibit TNBC cell expressed IL-6 and investigated the potential for classical IL-6 pathway induced signaling within TNBC cells. A panel of TNBC cell lines (MDA-MB-231, Hs578T, MDA-MB-468) was used. Enzyme linked immunosorbent assays (ELISA) revealed that C10 and COB-141 inhibit MDA-MB-231 cell IL-6 secretion, with COB-141 being ∼6.5 times more potent than C10. Therefore, the remainder of the study focused on COB-141 which inhibited IL-6 secretion, and was found, via quantitative real time polymerase chain reaction (QRT-PCR), to inhibit IL-6 mRNA in the TNBC panel. COB-141 had little, if any, effect on metabolic activity indicating that the IL-6 inhibition is not via a toxic effect. Flow cytometric analysis and QRT-PCR revealed that the TNBC cell lines do not express the IL-6 receptor (IL-6Rα). Trans-AM assays suggested that COB-141 exerts its inhibitory effect, at least in part, by reducing NF-κB (p65/p50) DNA binding. In summary, COB-141 is a potent inhibitor of TNBC cell expressed IL-6 and the inhibition does not appear to be due to non-specific toxicity. The TNBC cell lines do not have an intact classical IL-6 signaling pathway. COB-141's inhibitory effect may be due, at least in part, to reducing NF-κB (p65/p50) DNA binding.