Middle aged adults with low birth weight present with a higher chance of obesity and diabetes. Children that are born under six pounds were 1.27 times more likely to develop diabetes compared to babies born at a healthy weight over six pounds. Growth hormone (GH) therapy at a certain dose induced catch-up of lean body mass (LBM). However percentage body fat decreased in the GH-treated subjects. Bone mineral density SDS measured by DEXA increased significantly in the GH-treated group compared to the untreated subjects, though there is much debate over whether or not SGA (small for gestational age) is significantly adverse to children to warrant inducing catch-up. Babies that have a low birth weight are thought to have an increased risk of developing type 2 diabetes in later life. Low birth weight is linked with increase rates of obesity, insulin resistance, and type 2 diabetes and it is shown that children with the low birth weights have increased leptin levels after they catch up growth during childhood. Adiponectin levels are positively related with birth weight and BMI in babies with an increase of risk of type 2 diabetes. The leptin and adiponection mechanisms are still being studied when involving low birth weight. Around the world
There is much variation regarding birth weight within continents, countries, and cities. Even though over 20 million babies are born each year with low birth weight, it is hard to know the exact number as more than half of babies born in the world are not weighed at birth.
Mogamulizumab, sold under the brand name Poteligeo, is a humanized, afucosylated monoclonal antibody targeting CC chemokine receptor 4 (CCR4). The  U.S. Food and Drug Administration (FDA) approved it in August 2018 for treatment of relapsed or refractory mycosis fungoides and Sézary disease. It was approved in Japan in 2012, for the treatment of relapsed or refractory CCR4+ adult T-cell leukemia/lymphoma (ATCLL) and in 2014, for relapsed or refractory CCR4+ cutaneous T cell lymphoma (CTCL). The latter approval was based on study with 28 subjects.The precursor to mogamulizumab was a mouse anti-human CCR4 IgG1 mAb (KM2160), that was made in 1996 in a collaboration between Kouji Matsushima of University of Tokyo and Kyowa Hakko Kirin. Kyowa humanized it, and expressed the humanized gene in a CHO cell line in which FUT8 had been knocked out, which produced antibodies with no fucose in the Fc region. This is thought to enhance its antibody-dependent cell-mediated cytotoxicity. It was first tested in humans in 2007.Kyowa licensed rights for use outside of cancer to Amgen in 2008, for $100 million up front and $420 million in biodollars. Amgen ran a Phase I study to explore its use in asthma. Amgen terminated the agreement in 2014.As of 2014, there were reports that mogamulizimab can cause serious skin rashes and some cases of Stevens–Johnson syndrome.In 2017, the US FDA granted it a priority review for CTCL. Full approval was granted in August 2018. The U.S. Food and Drug Administration (FDA) considers it to be a first-in-class medication.