Background: Serotonin may have proliferative effects on neuroendocrine tumors (NETs). Inhibition of tryptophan hydroxylase (TPH), with resulting reduction of serotonin, may impact tumor size and growth (TG) in patients with NETs. We investigated the effects of TPH inhibitor telotristat ethyl (TE) on TG among patients receiving TE in clinical practice. Methods: A chart review study of 200 patients who had initiated TE was conducted. All patients had ≥2 radiological scans in the past 12 months prior to TE initiation and ≥1 scan post-TE initiation. Data were collected via a secure online portal. Descriptive statistics summarized physician and patient characteristics, and documented background NET treatment (i.e., somatostatin analog [SSA] and/or non-SSA). Longitudinal analyses of TG were assessed using a generalized linear regression model after controlling for documented background NET treatment and time since first scan. Results: Most physicians (71/114) were community-based oncologists. On average, patients were 61 ± 10 years old when initiating TE, 57% male, and 74% white; 61% had well-differentiated tumor with 61% of gastrointestinal origin. Patients received TE for an average of 12.0 ± 7.3 months and 82% (n = 163) were still receiving TE treatment at the time of data collection. The mean time from first scan to TE initiation was 5.6 ± 4.7 months and from TE initiation to last scan was 7.2 ± 6.3 months. Significant mean reductions in tumor size, after TE initiation, of 0.6 cm (p = 0.006) and TG of 8.5% (p = 0.045) were observed. Documented background NET treatment prior to initiating TE and time since first scan were not significant predictors of TG reduction. Results were consistent in a subset (n = 65) of patients who had no change in documented background NET treatment before and after initiating TE (mean reductions in tumor size 0.6 cm, p = 0.044 and TG 8.1%, p = 0.203). Conclusions: Treatment with TE may impact TG in patients with NETs. Prospective clinical studies are warranted to further examine the antiproliferative effects of TE.