The bis(triphenylarsane) complex of the [P4]2+ dication has been formed in a high‐yielding one‐pot synthesis. X‐ray crystallography reveals a butterfly structure of the bicyclo[1.1.0]‐tetraphosphane‐1,4‐diium core, with two triphenylarsane ligands in an exo,exo configuration (see picture). The reaction of [(Ph3As)2P4]2+ with Ph3P results in the quantitative formation of [(Ph3P)2P4]2+ and Ph3As.

Compound Ph3 As(OTf)2 as a pentacoordinated As(V) Lewis acid readily forms dicationic Lewis acid/base adducts upon addition of various Lewis bases. It also represents a stronger chloride-abstracting agent than Me3 SiOTf and facilitates the reductive coupling of PCl3 in the presence of AsPh3 to the unprecedented cation [P7 (AsPh3 )3](3+) as triflate salt. This crystallographically characterized nortricyclane-type cation represents a P7 R3 -derivative with the most electron-withdrawing substituents, resulting in a pronounced effect on the structural parameters of the P7 core.

Der Bis(triphenylarsan)‐Komplex des [P4]2+‐Dikations bildet sich in hoher Ausbeute bei einer Eintopfsynthese. Röntgenstrukturanalyse zeigt eine Schmetterlingsstruktur des Bicyclo[1.1.0]‐tetraphosphan‐1,4‐diium‐Kerns mit zwei Triphenylarsan‐Liganden in einer exo,exo‐Konfiguration (siehe Bild). Die Reaktion von [(Ph3As)2P4]2+ mit Ph3P ergibt quantitativ [(Ph3P)2P4]2+ und Ph3As.

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There are concerns about central nervous system (CNS)-replication of HIV-1 in patients on boosted protease inhibitors. Purpose of this study was to compare HIV-1 viral loads (VLs) from patients treated with only boosted dual protease inhibitor (bdPI), versus combination antiretroviral therapy (cART group), containing two nucleoside analogue reverse transcriptase inhibitors (NRTI) and a third partner. All patients from a large German HIV-treatment cohort with available medication, clinical and demographic data, including results from simultaneous HIV-1 viral load (VL) assessments in cerebrospinal fluid (CSF) and blood plasma, were retrospectively evaluated as controlled cross-sectional study. CSF had been obtained from patients with variable neurological symptoms during 2005-2014. Statistical analysis comprised nonparametric tests, regression and correlation techniques accounting for undetectable quantifications. Statistical analysis comprised nonparametric tests, regression and correlation techniques accounting for undetectable quantifications. Overall, 155 patients were evaluable (bdPI: 24; cART: 131). At time of CSF-collection, both groups were comparable in age, gender, CD4-cell counts, or primary HIV-transmission risks, though bdPI patients were clinically more advanced. The proportion of patients with undetectable HIV-1 (<50 copies/ml) in CSF was lower for bdPI group (25 vs 49.6 %; p = 0.026), but similar in plasma (46 vs 41 %). Median CSF-VL was higher in bdPI group (600 vs 50 copies/ml; p = 0.027) and similar in plasma. Mean VL CSF/plasma ratio was 342.91 for bdPI- and 54.48 for cART patients (p < 0.001). Pearson's regression analysis revealed a trend for an elevated VL-ratio over time within bdPI group. HIV-1 replication was higher and more frequently detectable in CSF from bdPI patients, indicating a worse CNS penetration effectiveness of used boosted PI. Within bdPI group, measured CNS-viral replication was increasing over time, suggesting an over time impaired HIV-1 suppression in CSF.