The clinical anti‐vascular endothelial growth factor (anti‐VEGF) drugs and metronomic chemotherapy (MET) induced tumor vascular normalization treatment (TVNT) are easily antagonized by tumor microenvironment metabolic cross‐talk between tumor cells and endothelial cells (ECs). To overcome this dilemma, nanodrug with the ability of ECs targeted glycolysis inhibition and nanodrug with the ability of tumor cell glycolysis inhibition, anti‐VEGF, and MET are combined to prepare Nano‐combination the pathways related to angiogenesis, tumor cell proliferation, and immunosuppression and breaking the negative sugar‐lipid‐protein metabolism balance in tumor microenvironment. Thus, stronger and more lasting normalized tumor vascular network and remarkable antitumor efficacy are obtained after treatment, constructing a positive feedback loop between TVNT and anti‐tumor therapy. Above all, this study provides a new insight for solving the bottleneck of clinical TVNT.

C43H78CaO22S2, monoclinic, P21 (no. 4), a = 18.2539(3) Å, b = 15.3118(3) Å, c = 18.3718(4) Å, β = 91.2637(17)°, Z = 4, V = 5133.65(18) Å3, Rgt(F) = 0.0544, wRref(F2) = 0.1622, T = 293(2) K.

Abstract-Efonidipine is a dual blocker of T-type and L-type calcium channels with 1, 4-dihydropyridine structure attached to a phosphonate skeleton. As a chiral compound, it has a special property that can exist as a racemic conglomerate or a racemic compound based on the different crystallization conditions. One racemic conglomerate and one racemic compound were disclosed and characterized in this research. Efonidipine conglomerate could obtain from its racemic solution when ethanol, methanol, tetrahydrofuran, ethyl acetate and acetonitrile were chosen as the crystallized solvent. While, racemic compound which existed as an acetone solvate could be prepared by crystallization from acetone only and the crystallization process must be keep stood without agitating. In order to confirm this conclusion, three single crystals of R-efonidipine, S-efonidipine and R/S-efonidipine acetone solvate have been prepared and determined.

Targeted Drug Delivery In article 2102724 by Jing Yao and co‐workers, blocking the metabolic crosstalk between tumor cells and tumor vascular endothelial cells through nano‐combination of LP and PP brings a new way to break through the predicament of tumor vascular normalization therapy. LP and PP are tacit companions to repair the tumor blood vessels.

Candida albicans (C. albicans) is a ubiquitous clinical fungal pathogen. In recent years, combination therapy, a potential treatment method to overcome C. albicans resistance, has gained traction. In this study, we synthesized a series of cyclometalated iridium(III) complexes with the formula [Ir(C-N)2(tpphz)](PF6) (C-N = 2-phenylpyridine (ppy, in Ir1), 2-(2-thienyl)pyridine (thpy, in Ir2), 2-(2,4-difluorophenyl) pyridine (dfppy, in Ir3), tpphz = tetrapyrido[3,2-a:2',3'-c:3'',2''-h:2''',3'''-j]phenazine) and polypyridyl ruthenium(II) complexes with the formula [Ru(N-N)2(tpphz)](PF6)2 (N-N = 2,2'-bipyridine (bpy, in Ru1), 1,10-phenanthroline (phen, in Ru2), 4,7-diphenyl-1,10-phenanthroline (DIP, in Ru3)), and investigated their antifungal activities against drug-resistant C. albicans and their combination with fluconazole (FLC). Of which, the combination of the lead iridium(III) complex Ir2 and FLC showed strong antifungal activity against drug-resistant C. albicans. Mechanism studies have shown that they can inhibit the formation of hyphae and biofilm, damage mitochondrial function and accumulate intracellular ROS. Therefore, iridium(III) complexes combined with FLC can be used as a promising treatment to exert anti-drug-resistant C. albicans activity, in order to improve the treatment efficiency of fungal infection.