In looking to recently emerging treatments and to those in development, there are a number of good possibilities. If it truly has less renal toxicity than tacrolimus, voclosporin seems to be a very good addition to the treatment armamentarium for lupus nephritis. I will be eager to see whether voclosporin works as well in the community as it did in the phase 3 AURORA trial. A key question will be: How long can patients use voclosporin before they start to experience some of the side effects? If these side effects (eg, rising creatinine and hypertension) are emerging after 6 to 12 months of use, that would be similar to what we have seen with tacrolimus.

In the past, I had not been terribly enthusiastic about prescribing belimumab for my patients with lupus nephritis, but I changed my mind after seeing the most recent data, and I do like using it in those with non-nephritis lupus. It works in at least 50% of my patients who start on it, and many of them stay on it for years. It does not increase the infection risk much over background therapy. Unfortunately, there is no oral form of belimumab; however, with the newer data, I was excited by the kidney protection it afforded. The BLISS-LN trial was run for 2 years, which is very admirable, and, as noted by Furie and colleagues, the risk of a renal-related event during the trial was almost 50% lower among patients who received belimumab than among those who received standard therapy alone.

There are many agents with phase 2 data. I am particularly interested in the studies of obinutuzumab, which, like rituximab, targets CD20. With rituximab, hypogammaglobulinemia and inactivating antibodies can develop. In addition, allergic reactions may develop as you approach, say, 3 to 4 years of treatment. Obinutuzumab is promising in that it is more B-cell depleting and less immunogenic than rituximab. The phase 2 trial looked very promising, so we shall see.

The monoclonal antibody anifrolumab is also of interest, and our group participated in one of the trials. Early data suggest that it may be particularly good for skin manifestations. I have not been too enthusiastic about agents that work on the Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway (eg, baricitinib and the Bruton tyrosine kinase inhibitor fenebrutinib) based on what I have seen thus far. The advantage of the JAK/STATs would be the oral route. Now, BIIB059, which is an antibody against the BDCA2 receptor on the dendritic cell, is quite interesting. I think that the data look quite good. That is a whole new approach and should really reduce the type I interferon production by the plasmacytoid dendritic cell.

Finally, telitacicept is another agent to watch, as it interferes with APRIL and BAFF, and that can be considered either positive or negative. In earlier studies with other similar drugs, there was a problem with infections and/or the agents did not work as well as belimumab. However, telitacicept looks quite good, and it is on an accelerated track at the US Food and Drug Administration for approval. I have not seen phase 3 data, and we will have to wait and see whether inhibiting both of these molecules results in increased infection.