Analysis of Growth Velocity in Children with Attention-Deficit/Hyperactivity Disorder Treated for up to 12 Months with Serdexmethylphenidate/Dexmethylphenidate

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Analysis of Growth Velocity in Children with Attention-Deﬁcit/

Hyperactivity Disorder Treated for up to 12 Months

with Serdexmethylphenidate/Dexmethylphenidate

Ann C. Childress, MD,

Andrew J. Cutler, MD,

2,3

Maitrey Patel, RPh,

and Charles Oh, MD

Abstract

Objective: Serdexmethylphenidate/dexmethylphenidate (SDX/d-MPH) is approved for the treatment of patients aged

‡6 years with attention-deﬁcit/hyperactivity disorder (ADHD). A 12-month, open-label safety study with SDX/d-MPH in

children with ADHD showed that SDX/d-MPH was well tolerated and comparable with other methylphenidate products. In

this post hoc analysis of the 12-month study, the objective was to characterize the effect of SDX/d-MPH on growth in children

with ADHD over 12 months.

Methods: This was a post hoc analysis of a dose-optimized, open-label, phase 3 safety study of SDX/d-MPH in children aged

6–12 years with ADHD (NCT03460652). Weight and height Z-score analyses were conducted. Z-score change from baseline

was calculated based on the baseline values for the subjects remaining in the study at the observation time point.

Results: Subjects (N = 238) from the treatment-phase safety population included all enrolled subjects who received ‡1doseof

study drug and had ‡1 postdose safety assessment. During treatment, the mean weight and height Z-scores decreased over time from

their respective baselines. At the 12-month time point, mean (standard deviation [SD]) Z-score changes from baseline for weight

and height for the subjects remaining in the study were -0.20 (0.50) and -0.21 (0.39), respectively; however, these mean changes in

Z-scores were not clinically signiﬁcant (change <0.5 SD). Long-term treatment with SDX/d-MPH was associated with modest

reductions in expected weight and lower-than-expected increases in height: effects that plateaued or diminished later in treatment.

Conclusion: The overall effects of SDX/d-MPH on growth velocity (the change in weight and height from one time point to

the next) were minimal, and the range of changes was not considered clinically signiﬁcant. ClinicalTrials.gov identiﬁer:

NCT03460652.

Keywords: ADHD, Azstarys, SDX/d-MPH, growth velocity, Z -score

Introduction

ethylphenidate (MPH) is a commonly prescribed medi-

cation for attention-deﬁcit/hyperactivity disorder (ADHD)

because of its efﬁcacy for symptom reduction and overall favorable

safety record. MPH is often prescribed for long-term use in patients

with ADHD (Storebø et al. 2018; Krinzinger et al. 2019). Serdex-

methylphenidate (SDX) is a prodrug of dexmethylphenidate (d-

MPH) and is coformulated with immediate release d-MPH in ﬁxed

molar dose ratios of 70% SDX:30% immediate release d-MPH

hydrochloride (HCl).

This formulation of SDX/d-MPH (Azstarys; Corium, LLC,

Boston, MA) was approved by the US Food and Drug Adminis-

tration for patients aged 6 years and older with ADHD.

Center for Psychiatry and Behavioral Medicine, Las Vegas, Nevada, USA.

SUNY Upstate Medical University, Syracuse, New York, USA.

Neuroscience Education Institute, Lakewood Ranch, Florida, USA.

Corium, LLC, Boston, Massachusetts, USA.

Funding: Clinical research was funded by Zevra Therapeutics (previously KemPharm, Inc.). Funding for editorial and writing assistance in the form of

proofreading, copyediting, and fact-checking was provided by Corium, LLC.

Data contained in this article were previously presented at the Annual Meeting of the American Academy of Child and Adolescent Psychiatry

(AACAP) Virtual Conference, October 19–24, 2020.

ª Ann C. Childress et al. 2023; Published by Mary Ann Liebert, Inc. This Open Access article is distributed under the terms of the Creative Commons

License [CC-BY] (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided

the original work is properly cited.

JOURNAL OF CHILD AND ADOLESCENT PSYCHOPHARMACOLOGY

Volume 33, Number 4, 2023

Mary Ann Liebert, Inc.

Pp. 134–142

DOI: 10.1089/cap.2023.0012

134

In a pivotal, randomized, placebo-controlled, double-blind lab-

oratory classroom study of children with ADHD, SDX/d-MPH

treatment was shown to signiﬁcantly improve ADHD symptoms

compared with placebo (Kollins et al. 2021). SDX/d-MPH onset

began by 30 minutes postdose, and the treatment effect lasted up to

13 hours. Adverse events (AEs) were similar to other stimulants

used for the treatment of patients with ADHD.

A subsequent, 1-year, open-label safety study of SDX/d-MPH in

children with ADHD showed that SDX/d-MPH was well tolerated

and had sustained efﬁcacy during the 1-year treatment period

(Childress et al. 2023). Of the 238 subjects assessed in the 1-year

study, the most common treatment-emergent AEs were decreased

appetite (18.5%), upper respiratory tract infection (9.7%), naso-

pharyngitis (8.0%), decreased weight (7.6%), and irritability

(6.7%).

Long-term treatment with stimulants, such as MPH for ADHD,

in children has been associated with modest slowing of growth

velocity and prescribing information for these treatments warns of

long-term growth suppression, which can cause concern and limit

their use (Spencer et al. 2006; Faraone and Giefer 2007; Krinzinger

et al. 2019). The objective of the current investigation was to

characterize the effects of SDX/d-MPH on growth in children with

ADHD treated with SDX/d-MPH from the 1 year, open-label,

safety study (Childress et al. 2023).

Methods

This post hoc analysis of a dose-optimized, open-label, phase 3

safety study of SDX/d-MPH in children aged 6–12 years with

ADHD (NCT03460652) (Childress et al. 2023) was conducted at

18 sites in the United States. The original study protocol and

amendments were approved by an institutional review board before

each center initiated the study. The ﬁrst patient was screened on

February 21, 2018, and the last follow-up visit was on June 27, 2019.

Subjects

The subjects were children aged 6–12 years with ADHD at the

start of the dose-optimization (DO) phase of the study. Subjects

included those rolled over from the antecedent pivotal study

(Kollins et al. 2021) within 45 days of their last dose of SDX/d-

MPH, and new subjects who did not participate in the pivotal study

or who entered the trial more than 45 days after their last dose in the

pivotal study (Childress et al. 2023). Subjects had to have a body

weight of at least 21 kg at the screening phase and be in good health.

At least one parent or legal guardian was required to provide written

permission, and each subject had to give written or verbal per-

mission for study participation.

Study design

The study design included a 30-day screening phase, a 3-week

DO phase, a 360-day treatment phase, and a follow-up visit. Only

new subjects underwent screening and DO. During the DO phase,

new subjects were titrated to their optimized dose based on the best

dose response and individual tolerability to the treatment (Childress

et al. 2023).

New subjects started treatment with the 39.2/7.8 mg dose of

SDX/d-MPH daily, which is a molar equivalent to 30 mg of to-

tal d-MPH HCl, for 7 days. If needed, dose adjustments were

performed based on the investigator’s assessment of the subject

at weekly intervals. The SDX/d-MPH dose could be increased

to 52.3/10.4 mg (40 mg molar equivalent of total d-MPH HCl),

decreased to 26.1/5.2 mg (20 mg molar equivalent of total d-MPH

HCl), or maintained at the same dose for the next week of dosing.

The dose at the end of the third week was assigned as the opti-

mized dose. Subjects who rolled over from the pivotal study re-

mained on their optimized dose from that study. The optimized SDX/

d-MPH dose was used during the treatment phase. All subjects were

administered 1 capsule daily of their optimized dose of SDX/d-MPH.

Weight and height analyses were conducted in the treatment phase

safety population of enrolled subjects. This population included

those who received at least 1 dose of study medication and had at

least 1 postdose safety assessment in the treatment phase. Com-

pleters are those subjects that completed 12 months of treatment.

Weight and height measurements

Body weight (in kg) and height (in cm) were measured at each

monthly visit. Body weight was measured using a calibrated scale

while subjects remained in their normal clothing, with shoes and

jacket (and/or outer clothing) removed. Height was measured using

a stadiometer with the subject’s shoes removed.

Assessments

The predicted weight and height for each subject and visit were

calculated based on the United States 2000 Centers for Disease

Control (CDC) Growth Charts (ages 2 to <20 years) (Kuczmarski

et al. 2002), using each subject’s observed baseline weight or

height. The predicted weight and height assumed maintenance of

baseline weight and height percentile for each subject. The pre-

dicted weight and height over time were used as references to assess

the trajectory of the observed weight and height over time.

Z-score, which expresses an anthropometric value as the number

of standard deviations (SDs) below or above the mean of a refer-

ence population, was calculated for each subject at each visit. The

reference population was based on the United States 2000 CDC

Growth Charts (ages 2 to <20 years) (Kuczmarski et al. 2002).

Z-scores were assessed against the reference population for both

weight and height (Kuczmarski et al. 2002), as follows:

Z  score ¼

observed value  mean of the reference population

SD of the reference population

A Z-score change <0.5 SD is considered not clinically signiﬁ-

cant. Z-score change from baseline was calculated based on the

baseline values for the subjects remaining in the study at the ob-

servation time point. Percentiles were assessed as the percentage of

observations that fell below a certain value for the reference popu-

lation. Z-score by baseline body mass index (BMI) quartile was

calculated based on the following baseline BMI quartiles: quartile 1,

BMI £16.1; quartile 2, BMI >16.1 to £17.8; quartile 3, BMI > 17.8

to £21.6; quartile 4, BMI >21.6.

The descriptive statistics included number of subjects (n), mean,

SD, standard error, and Z-score. No statistical tests were conducted.

Results

Subject disposition

Subject disposition has been previously described (Childress

et al. 2023). Brieﬂy, 323 subjects were screened, among whom 282

were enrolled in the study. Of the 282 enrolled subjects, 254 entered

the treatment phase (which included 70 rollover subjects and

184 new subjects), of whom 238 subjects were included in the

treatment phase safety population (Fig. 1).

GROWTH VELOCITY IN CHILDREN TREATED WITH SDX/

D-MPH 135

Subject demographics and baseline characteristics

The mean (SD) age for the subjects was 9.1 (1.9) years; 60.9% of

the subjects were male, and 39.1% were female. The mean (SD;

minimum, maximum) for weight was 38.6 (13.9; 21.0, 97.0) kg,

BMI was 19.2 (4.6; 13.1, 37.5) kg/m

, and height was 139.6 (11.9;

113.5, 171.2) cm (Table 1). Additional subject characteristics have

been previously reported (Childress et al. 2023).

Growth velocity

Weight. The mean (SD) body weight at baseline was

38.6 (13.9) kg with a Z-score of 0.74 (1.13) (Table 2), indicating a

baseline weight higher than the mean expected body weight for the

reference population. In the ﬁrst 30 days after initiating the treat-

ment phase, mean observed weight decreased slightly, and this was

followed by 2 months of slowdown in observed weight gain

(Fig. 2A). After this slowdown, a steady increase in observed body

weight paralleled the predicted weight curve, but at a lower starting

point because of the weight deﬁcits in the study population during

the ﬁrst 3 months.

At 90 days, the mean observed weight and predicted weight were

38.5 and 40.2 kg, respectively, with a difference between the means

of 1.7 kg. At the end of the study (360 days), the mean observed

weight and predicted weight were 41.1 and 42.8 kg, respectively,

with the same difference between the means of 1.7 kg as after

3 months of treatment.

The mean (SD) weight Z-score at baseline was 0.74 (1.13). Mean

weight Z-score decreased during the ﬁrst month in the treatment

phase, as evidenced by the decline at 30 days (Fig. 2B). Most of the

mean weight Z-score decline occurred in the ﬁrst 4 months of

treatment and remained stable thereafter, near 0.5. For all subjects,

the mean (SD) weight Z-score during the ﬁrst 3 months was

0.53 (1.17), and at 12 months, it was 0.51 (1.08), a change from

baseline of -0.22 (0.31) at 3 months and -0.20 (0.50) at 12 months

based on the baseline scores for those subjects remaining in the

study at 3 and 12 months, respectively.

For subjects who completed the study, smaller decreases or

lower-than-expected increases were observed during the second

and third months, after which the weight velocity resumed, al-

though at a lower starting weight at 90 days. The average weight

decreased from the 68.4 (27.4) percentile to the 64.3 (28.8) per-

centile during the ﬁrst month in the treatment phase, with an ad-

ditional small decrease to the 62.8 (27.7) percentile by 12 months

(Fig. 2C).

Approximately the same mean weight percentile was maintained

for the remainder of the study. The percentage of subjects with

clinically notable weight loss, deﬁned as a weight decrease from

baseline >7%, was 8.7% at 30 days. The percentage of subjects with

weight loss increased over time, peaking at 14.5% of subjects at

4 months and then declining to 5.2% of subjects at the end of the

study (360 days). This time course is consistent with average

weight loss observed during the beginning of the treatment phase

followed by weight gains later in the study.

The mean weight Z-scores over time by baseline BMI quartiles

are shown in Figure 3. The mean baseline Z-scores were -0.40,

0.32, 0.92, and 2.16, for baseline BMI quartiles 1, 2, 3, and 4,

respectively. At the end of treatment, the mean Z-scores were

-0.46, 0.12, 0.55, and 1.95, a change from baseline of -0.07, -0.13,

-0.33, and -0.25 for baseline BMI quartiles 1, 2, 3, and 4, re-

spectively.

The Z-scores for subjects with a baseline BMI <16.1 kg/m

ap-

proached the baseline Z-score by the end of the study after a de-

crease in weight Z-score during the initial 3 months of treatment.

The weight Z-score of subjects with mean BMI > 21.6 kg/m

baseline decreased during the initial 2 months of treatment and

remained approximately constant thereafter.

Height. The mean (SD) height at baseline was 139.6 (11.9) cm

with a Z-score of 0.54 (0.98) (Table 2), indicating that the baseline

height was higher than the mean expected body height for the

reference population (i.e., the subjects in the present study were

FIG. 1. Subject disposition.

Table 1. Subjects’ Demographics. Treatment Phase

Safety Population

Parameter Total (N = 238)

Age, years

Mean (SD) 9.1 (1.87)

Minimum, maximum 6, 12

Sex, n (%)

Male 145 (60.92)

Female 93 (39.08)

Weight, kg

Mean (SD) 38.6 (13.9)

Minimum, maximum 21.0, 97.0

Height, cm

Mean (SD) 139.6 (11.92)

Minimum, maximum 113.5, 171.2

Body mass index, kg/m

Mean (SD) 19.2 (4.6)

Minimum, maximum 13.1, 37.5

SD, standard deviation.

Table 2. Baseline Observed Mean Body Weight

and Height, Predicted Weight and Height, Weight

and Height Z-Score, and Weight and Height

Percentiles: Treatment Phase Safety Population

Parameter, mean (SD)

Weight (kg),

n = 238

Height (cm),

n = 238

Observed 38.6 (13.9) 139.6 (11.9)

Predicted 38.6 (13.9) 139.6 (11.9)

Z-score 0.74 (1.13) 0.54 (0.98)

Percentile 68.4 (27.4) 64.9 (26.6)

SD, standard deviation.

136 CHILDRESS ET AL.

FIG. 2. Mean observed body weight versus mean predicted body weight (A), mean weight Z-score by completion status (B), and mean

body weight percentile (C). Treatment phase, safety population. All subjects: n = 238. Completers: n = 155. The black curve represents

all subjects remaining in the study at each visit (completers + drop-outs before they dropped out). The red curve represents completers

who are subjects that completed 12 months of treatment. Bars are standard error.

137

taller than the expected height for their age, according to CDC

norms).

A comparison of observed height versus predicted height

showed a steady increase of the mean observed height over time,

which was at a lower rate than the predicted velocity of height gain

at each monthly visit (Fig. 4A). In the treatment phase at 90 days,

the mean observed height and predicted height were 140.8 and

141.4 cm, respectively, with a difference between the means of

0.6 cm. At 180 days, the mean observed height and predicted height

were 141.8 and 142.7 cm, respectively, with a difference between

the means of 0.9 cm. At the end of the study, the mean observed

height and predicted height were 143.4 and 144.8 cm, respectively,

with a difference between the means of 1.4 cm.

Mean height Z-scores decreased over time (Fig. 4B). The mean

(SD) baseline height Z-score for all subjects was 0.54 (0.98). The

greatest mean Z-score decrease occurred at 6 months. The mean

height Z-score decreased to 0.39 (0.98) after 6 months in the

treatment phase, a change from baseline of -0.14 (0.28), and de-

creased to 0.24 (0.96) after 12 months, a change from baseline of

-0.21 (0.39), based on the baseline scores for those subjects re-

maining in the study at 6 and 12 months, respectively.

Mirroring the mean height Z-score, the mean height percentile

steadily decreased, with the mean (SD) height percentile decreasing

from the 64.9 (26.6) to the 60.7 (27.7) percentile after 6 months in

the treatment phase and to the 57.0 (27.7) percentile at 12 months

(Fig. 4C).

The mean baseline height Z-scores were 0.18, 0.53, 0.51, and

0.96, for baseline BMI quartiles 1, 2, 3, and 4, respectively (Fig. 5).

At the end of treatment, the mean Z-scores were -0.11, 0.16, 0.19,

and 0.79, a change from baseline of -0.25, -0.25, -0.23, and -0.04,

FIG. 3. Mean weight Z-score by baseline BMI quartile. Treatment phase, safety population. Bars are standard error. BMI, body mass

index.

138 CHILDRESS ET AL.

FIG. 4. Mean observed height versus mean predicted height (A), mean height Z-score by completion status (B), and mean height

percentile (C). Treatment phase, safety population. All subjects: n = 238. Completers: n = 155. The black curve represents all subjects

remaining in the study at each visit (completers + drop-outs before they dropped out). The red curve represents completers who are

subjects that completed 12 months of treatment. Bars are standard error.

139

for baseline BMI quartiles 1, 2, 3, and 4, respectively. The mean

height Z-score decrease from baseline was much lower in the

baseline BMI quartile 4 (which also had a higher mean baseline

height Z-score) than in the lower 3 baseline BMI quartiles.

Discussion

The safety and tolerability results from this 1-year open-label

study of SDX/d-MPH in children with ADHD have been previously

reported (Childress et al. 2023). Decreased weight was reported as a

treatment-emergent AE, occurring in 7.6% of subjects. In this

analysis, baseline mean weight and height were higher in study

subjects than in the reference population.

Other studies of MPH in children with ADHD also observed

similarly higher baseline weight and height than their reference

samples (Swanson et al. 2006; Childress et al. 2022). In this anal-

ysis, we showed a transient decrease in observed body weight

followed by a slower-than-predicted weight gain in the ﬁrst

3 months of SDX/d-MPH treatment. Subsequently, the resulting

difference between observed and predicted mean body weights

remained fairly constant to the end of the treatment phase. In the

present study, the change in weight Z-score from baseline to the

study’s end at 12 months was -0.20.

A Z-score change <0.5 SD is considered not clinically signiﬁ-

cant. The mean weight Z-score decreased initially, with the largest

mean Z-score decrease occurring during the ﬁrst month of the

treatment phase, with smaller decreases in the second and third

month. These results are consistent with published data, suggesting

that the rate of accumulating weight deﬁcits is attenuated over time

with continued stimulant treatment (Faraone et al. 2008).

FIG. 5. Mean height Z-score by baseline BMI quartile. Treatment phase, safety population. Bars are standard error. BMI, body mass

index.

140 CHILDRESS ET AL.

The mean weight changes as a percent from baseline-by-

baseline BMI quartile groups showed that all four baseline BMI

quartile groups had an initial weight decrease during the ﬁrst to

fourth months in the treatment phase, with a notable smaller and

shorter weight decrease in baseline BMI quartile 1 compared with

the other three baseline BMI quartile groups.

The relative weight gain after the initial decline through the end

of treatment was higher in subjects in the ﬁrst and second baseline

BMI quartile groups compared with subjects in the third and fourth

baseline BMI quartile groups. This difference in weight gain in-

dicates that subjects with a higher baseline BMI experienced a

larger initial reduction in weight gain than subjects with a lower

baseline BMI. Relative weight gain after *3 months of treatment

appeared similar between all baseline BMI quartiles.

With respect to height, the positive mean baseline height Z-score

of 0.54 for all study subjects indicates that the average baseline

height was higher than the mean expected height for the reference

population. Mean height increased steadily during the study, al-

though the height increases were lower when compared against the

reference population. Mean height Z-scores and height percentiles

decreased over time.

The change in height Z-score from baseline to the end of the

study was -0.21. We also showed that the mean height Z-score

decrease from baseline was much lower in the upper baseline BMI

quartile group (-0.04 for fourth baseline BMI quartile) than in the

lower three baseline BMI quartiles (-0.25, -0.25, and -0.23 for

ﬁrst, second, and third baseline BMI quartile groups, respectively).

The effects of long-term treatment of stimulants on weight and

height in pediatric patients are well documented (Spencer et al.

2006; Swanson et al. 2006; Faraone et al. 2008, 2010). A 5-week

study of 253 children aged 6–12 years with ADHD receiving daily

doses of extended release d-MPH found that the percentage of

subjects with clinically notable weight loss (a weight decrease from

baseline >7%) was 5.8%, 4.0%, and 7.7%, after daily doses of 10,

20, and 30 mg extended release d-MPH (vs. 0% after placebo)

(Childress et al. 2009).

However, that study was of a much shorter span than the current

study, consisting of a 3-week dose optimization phase followed by

a 2-week maintenance phase, and it is possible that study had not

reached maximum effect on body weight that may have been

measured later in treatment had the treatment continued.

In a 21-month study with a dose-optimized long-acting MPH

formulation in 407 children aged 6–13 years with ADHD (Spencer

et al. 2006), the mean baseline weight Z-score was higher than 0,

indicating that the children in that study were on average heavier

than the CDC reference sample. In that study, the largest weight

Z-score decrease occurred during the ﬁrst 5 months of treatment

(decreased from 0.16 to -0.11) and then remained relatively stable

for the remainder of the study.

In a more recent 12-month open-label safety study of extended-

release MPH in children aged 4–5 years with ADHD, subjects

entering the study were heavier and taller than the reference pop-

ulation (Childress et al. 2022). Weight decrease was a commonly

reported treatment-emergent AE (Childress et al. 2022), as was

found in the 1-year safety study of SDX/d-MPH (Childress et al.

2023).

In the extended-release MPH study (Childress et al. 2022), de-

crease in weight-for-age percentiles was smallest for subjects in the

lowest quartile of baseline weight (-8.1) versus the other three

baseline weight quartiles (-14.0, -10.0, and -11.4 for second, third,

and fourth quartiles, respectively). In addition, the smallest changes

in height percentiles were seen for children in the ﬁrst quartile of

baseline height (-2.4), compared with the second (-10.0), third

(-8.7), and fourth (-9.7) baseline height quartiles.

The limitations of this study include the open-label nature of the

study design and the lack of a control placebo arm or a comparator

product. The analysis of a drug effect on body weight changes over

time by itself is limited because children are expected to grow and

gain weight as they age, even during SDX/d-MPH treatment. In

addition, some of the subjects who entered this study were not

stimulant naive, as some had been previously treated with SDX/d-

MPH in the antecedent pivotal study. Thus, previous stimulant

exposure may have impacted baseline height and weight measures,

resulting in an underestimate of growth velocity changes.

Conclusion

In this study, we show that long-term treatment for up to 1 year

with SDX/d-MPH was associated with modest reductions in ex-

pected weight and lower-than-expected increases in height, effects

that plateaued or diminished later in treatment. Although both

weight and height decreased compared with the reference popula-

tion, the decrease was less than what is clinically signiﬁcant.

Clinical Signiﬁcance

This phase 3 clinical trial of SDX/d-MPH in children aged

6–12 years showed that the overall effects of SDX/d-MPH on

growth velocity were minimal and changes were in a range con-

sidered not clinically signiﬁcant.

Acknowledgments

Medical writing support for the development of this manuscript,

under the direction of the authors, was provided by Gautam Bijur,

PhD, Charlette Tiloke, PhD, and editing support by Kathleen

Blake, PhD, all of Ashﬁeld MedComms, an Inizio company, and

funded by Corium, LLC.

Authors’ Contributions

All the authors were actively involved in data interpretation,

critical review of the data, article writing, and editing.

Disclosures

A.C.C serves as consultant for Aadrvark, Arbor, Aytu, Iron-

shore, Neos Therapeutics, Neurocentria, Noven, Otsuka, Purdue,

Rhodes, Sky, Sunovion, Tris Pharma, Zevra Therapeutics (previ-

ously KemPharm, Inc.), Supernus, Jazz, Corium, LLC, and Lumos.

She has served on the speaker’s bureau for Takeda (Shire), Arbor,

Ironshore, Neos Therapeutics, Tris Pharma, and Supernus. She has

received research support from Allergan, Takeda (Shire), Emalex,

Akili, Arbor, Ironshore, Lumos, Neos Therapeutics, Otsuka, Pur-

due, Adlon, Rhodes, Sunovion, Tris Pharma, Zevra Therapeutics

(previously KemPharm, Inc.), Supernus, US Food and Drug Ad-

ministration, and Servier. She has received writing support from

Takeda (Shire), Arbor, Ironshore, Neos Therapeutics, Purdue,

Rhodes, Sunovion, and Tris Pharma; She has served on advisory

boards for Takeda (Shire), Akili, Arbor, Cingulate, Ironshore, Neos

Therapeutics, Neurovance, Otsuka, Purdue, Adlon, Rhodes, Su-

novion, Tris Pharma, Supernus, NLS Pharma, and Corium, LLC.

A.J.C. is a consultant for AbbVie, Akili Interactive, Arbor

Pharmaceuticals, Atentiv, Axsome, Corium, LLC, Ironshore,

Neurosigma, Noven, Otsuka, Purdue Canada, Shire, Sunovion,

Supernus, Takeda, and Tris Pharma. He has served on speaker’s

GROWTH VELOCITY IN CHILDREN TREATED WITH SDX/

D-MPH 141

bureaus for AbbVie, Arbor Pharmaceuticals, Axsome, Corium, LLC,

Ironshore, Noven, Otsuka, Shire, Sunovion, Supernus, Takeda, and

Tris Pharma. He has received research support from Aevi Genomics,

Akili Interactive, Arbor Pharmaceuticals, Ironshore, Zevra Ther-

apeutics (previously KemPharm, Inc.), Otsuka, Purdue Canada,

Rhodes, Shire, Sunovion, Supernus, and Takeda. He is an employee

and board member of the Neuroscience Education Institute.

M.P. and C.O. are employees of Corium, LLC.

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Address correspondence to:

Charles Oh, MD

Corium, LLC

11 Farnsworth St., FL 4

Boston, MA 02210

USA

E-mail: [email protected]

142 CHILDRESS ET AL.