Discovery of 3-aminopicolinamides as metabotropic glutamate receptor subtype 4 (mGlu4) positive allosteric modulator warheads engendering CNS exposure and in vivo efficacy

Article abstract of DOI:10.1016/j.bmcl.2016.04.041

This letter describes the further chemical optimization of the picolinamide-derived family of mGlu₄ PAMs wherein we identified a 3-amino substituent to the picolinamide warhead that engendered potency, CNS penetration and in vivo efficacy. From

Full text of DOI:10.1016/j.bmcl.2016.04.041

Bioorganic & Medicinal Chemistry Letters 26 (2016) 2915–2919
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Bioorganic & Medicinal Chemistry Letters
journal homepage: www.elsevier.com/locate/bmcl
Discovery of 3-aminopicolinamides as metabotropic glutamate
receptor subtype 4 (mGlu4) positive allosteric modulator warheads
engendering CNS exposure and in vivo efficacy
Rocco D. Gogliotti a, Darren W. Engers a,b, Pedro M. Garcia-Barrantes a, Joseph D. Panarese a,
Patrick R. Gentry a, Anna L. Blobaum a,b, Ryan D. Morrison a, J. Scott Daniels a,b, Analisa D. Thompson a,
Carrie K. Jones a,b,d, P. Jeffrey Conn a,b,d, Colleen M. Niswender a,b,d, Craig W. Lindsley a,b,c,
,
⇑
Corey R. Hopkins a,b,c,
⇑
a Vanderbilt Center for Neuroscience Drug Discovery, Vanderbilt University Medical Center, Nashville, TN 37232, USA
b Department of Pharmacology, Vanderbilt University School of Medicine, Nashville, TN 37232, USA
c Department of Chemistry, Vanderbilt University, Nashville, TN 37232, USA
d Vanderbilt Kennedy Center, Vanderbilt University School of Medicine, Nashville, TN 37232, USA
a r t i c l e i n f o
a b s t r a c t
Article history:
This letter describes the further chemical optimization of the picolinamide-derived family of mGlu4 PAMs
wherein we identified a 3-amino substituent to the picolinamide warhead that engendered potency, CNS
penetration and in vivo efficacy. From this optimization campaign, VU0477886 emerged as a potent
(EC50 = 95 nM, 89% Glu Max) mGlu4 PAM with an attractive DMPK profile (brain:plasma Kp = 1.3), rat
CLp = 4.0 mL/min/kg, t1/2 = 3.7 h) and robust efficacy in our standard preclinical Parkinson’s disease
model, haloperidol-induced catalepsy (HIC).
Received 3 March 2016
Revised 14 April 2016
Accepted 15 April 2016
Available online 19 April 2016
Keywords:
mGlu4
Ó 2016 Elsevier Ltd. All rights reserved.
Metabotropic glutamate receptor
Positive allosteric modulator (PAM)
Parkinson’s disease
Structure–activity relationship (SAR)
Metabotropic glutamate receptor subtype 4 (mGlu4) has gar-
nered a great deal of interest as a novel, non-dopaminergic target
for the potential treatment of Parkinson’s disease (PD) by virtue of
selective activation via positive allosteric modulators (PAMs)1–6
and normalization of the overactive indirect pathway within the
basal ganglia circuitry.7,8 Beyond symptomatic treatment of motor
disturbances, emerging data suggests mGlu4 PAMs may also be neu-
roprotective, and hence disease-modifying.1–6 As discussed in the
field, SAR can be steep for certain allosteric chemotypes, and ade-
quate CNS penetration, as well as overall DMPK properties, have
been an ongoing challenge in the development of mGlu4 PAMs.6,9,10
An optimization program in our lab based on an HTS hit has afforded
a diverse array of picolinamide-based mGlu4 PAMs 1–5 (Fig. 1),11–15
and by surveying bioisosteres, the identification of our first preclin-
ical candidate, VU0418506 (6).16 Our back-up program sought to
distance from the pyrazolo[4,3-b]pyridine head group of 6, and
one aspect focused on functionalized picolinamides, leveraged en
route to 7.16 In this Letter, we will detail the discovery, SAR, DMPK
profiles and in vivo efficacy of the newly identified 3-aminopicoli-
namide mGlu4 PAM warheads.
In route to the pyrazolo[4,3-b]pyridine head group of
(EC50 = 67 nM, pEC50 = 7.17 0.07, 109.3 3.8% Glu Max), we had
synthesized and evaluated single 3-aminopicolinamide,
6
a
7
(EC50 = 587 nM, pEC50 = 6.24 0.03, 88.1 2.0% Glu Max) analog
(Fig. 2).16 While ꢀ7-fold less potent than 6, 7 represented a struc-
turally distinct and unexplored chemotype. Thus, we quickly pre-
pared a diverse set of either 3- or 4-functionalized picolinamides
8–15; however, all proved to be inactive as mGlu4 PAMs, suggest-
ing that the 3-amino moiety, and the presence of a hydrogen bond
donor, in 7 was a required pharmacophore.
We then elected to survey the 3-aminopicolinamide warhead in
the context of a broader array of Eastern moieties (e.g., imides,
aryl/heteroaryl, sulfonamides, ethers) previously shown to engen-
der mGlu4 PAM activity, maintaining a key meta-chloro moiety.
The chemistry to assemble analogs 17 was straight forward, as
the Eastern moieties (R = phthalimides, imides, lactams and ethers)
⇑
Corresponding authors.
E-mail addresses: craig.lindsley@vanderbilt.edu (C.W. Lindsley), corey.hopkins@
vanderbilt.edu (C.R. Hopkins).
http://dx.doi.org/10.1016/j.bmcl.2016.04.041
0960-894X/Ó 2016 Elsevier Ltd. All rights reserved.

2916
R. D. Gogliotti et al. / Bioorg. Med. Chem. Lett. 26 (2016) 2915–2919
potent (human and rat mGlu4 EC50s of 64.6 nM and 46.6 nM,
respectively) and also possessed favorable physicochemical prop-
erties (MW = 396, cLogP = 2.27 and TPSA = 103). However, before
locking into these two novel mGlu4 PAMs for more detailed
characterization, we wanted to fully evaluate other SAR within this
series of mGlu4 PAMs.
As the 3-aminopicolinamide moiety afforded potent mGlu4
PAMs, we then surveyed the activity of the corresponding
3-hydroxypicolinamide analog of 17a, 18 (Fig. 3). Compound 18
(mGlu4 EC50 = 125 nM, 115.4% Glu Max) proved to be of compara-
ble potency to 17a, but offered no advantage in terms of physio-
chemical properties. Then, in the context of 17t, we surveyed
alternative heteroaromatic amino amides, and found that the ison-
icotinamide derivative, 19, was devoid of mGlu4 PAM activity
O
O
Cl
O
S
O
O
N
H
N
N
Cl
N
H
N
H
Cl
1
2
, VU0364439
, VU0361737 (ML128)
O
N
H
N
O
O
O
N
N
O
Cl
N
H
Cl
N
H
Cl
3
4
, VU0366037
, VU0400195 (ML182)
(EC50 > 10
lM), while
a
pyrazine analog, 20, was active
(EC50 = 296 nM, 103.9% Glu Max), but lost ꢀ5-fold relative to 17t.
Therefore, we advanced both 17a and 17t in a battery of in vitro
and in vivo DMPK assays.11–16
For in vivo tool compounds, the in vitro and in vivo DMPK pro-
files of both 17a (VU0477886) and 17t (VU0483872) were attrac-
tive. PAM 17a displayed moderate intrinsic clearance in both rat
and human microsomes (CLHEP 51 mL/min/kg and 5.8 mL/min/kg,
respectively), limited free fraction (Fu (h, r) of 0.007 and 0.003)
H
F
N
O
N
N
Cl
N
H
N
H
Cl
N
6
5
, VU0418506
, VU0364770 (ML292)
Figure 1. Structures of picolinamide-based mGlu4 PAMs (1–5), and the first
preclinical candidate, VU0418506 (6).
and
IC50s > 30
a
mixed cytochrome P450 profile (3A4, 2D6 and 1A2
M, 2C9 IC50 = 7.2 M). In Sprague Dawley (SD) rats,
l
l
17a was a low clearance compound (CLP = 3.98 mL/min/kg) with
a low volume (Vss = 0.85 L/kg) and a 3.7 h half-life. In a rat
plasma:brain level (PBL) cassette study (0.25 mg/kg, 0.25 h, IV),
17a effectively partitioned into the CNS (Kp = 1.31) and was not a
human P-gp substrate (efflux ratio = 1.2). Similarly, PAM 17t dis-
played moderate to high intrinsic clearance in both rat and human
microsomes (CLHEP 46.1 mL/min/kg and 17.71 mL/min/kg, respec-
tively), limited free fraction (Fu (h, r) of 0.004 and 0.004) and a
have all previously been described11–15 and were available as func-
tionalized anilines 16a–d (Scheme 1).
The SAR for analogs 17 (Table 1) represented a departure from
simple picolinamides 1–5 or the pyrazolo[4,3-b]pyridine head
group of 6, displaying a steep phenotype. Phthalimides, such as
17a and 17d, displayed good PAM activity, as did certain isoin-
dolinones, such as 17e and 17h. However, electronics played a
key role in activity, as an electron-rich isoindolinone, 17h, pos-
sessed an EC50 of 319 nM, whereas an electron-deficient congener,
mixed cytochrome P450 profile (2C9 2D6 IC50s > 30
lM, 1A2
IC50 = 2.6 M and 3A4 IC50 = 21.1 M). In SD rats, 17t was a low
l
l
17g, was devoid of PAM activity (EC50 > 10 lM). This proved to be a
clearance compound (CLP = 13.7 mL/min/kg) with a uniform vol-
ume (Vss = 0.86 L/kg) and a 1.5 h half-life. In a rat PBL cassette
study (0.25 mg/kg, 0.25 h, IV) 17t displayed moderate partitioning
into the CNS (Kp = 0.36) and was not a human P-gp substrate
(efflux ratio = 1.9). Both 17a and 17t displayed excellent selectivity
versus the other mGlu receptors. Thus, both new PAMs possessed
acceptable profiles to advance into our standard rodent pharmaco-
dynamic model for Parkinson’s disease (PD), reversal of haloperi-
dol-induced catalepsy (HIC).11–16
PAM 17a (VU0477886) was evaluated first via an oral route of
administration in the HIC model (Fig. 4), and compared side-by-
side with the preclinical candidate, 6 (VU0418506). In this study,
a 1 mg/kg p.o. dose of 17a, proved to be as efficacious as 6 in
reversing a robust 1.5 mg/kg dose of haloperidol. As our previous
PBL study was IV, we also collected plasma and brain samples from
general trend (F and CN also devoid of PAM activity). Lactams 17j–s
also displayed a range of mGlu4 PAM activity, from inactive to
758 nM, driven mainly by lipophilicity and steric bulk. Here, only
two analogs, 17a, a phthalimide congener, and 17t, an ether deriva-
tive, displayed potency (EC50s below 100 nM) comparable to the
clinical candidate, 6. The unsubstituted phthalimide 17a was
potent at both human and rat mGlu4 (EC50s of 94.5 nM and
128 nM, respectively), and possessed attractive physicochemical
properties (MW = 392, cLogP = 2.52 and TPSA = 105 Å2). Similarly,
the chemically distinct, pyrimidinyl ether 17t was even more
H
N
NH2
N
O
F
N
Cl
N
H
Cl
N
H
N
R
R
NH2
O
7
, EC50 = 578 nM
6
, EC50 = 67 nM
a
N
H
Cl
H2N
Cl
N
Cl
O
O
F
O
Br
O
16
17
N
H
N
H
N
N
H
H
N
N
10
N
N
R1
8
9
11
R1
O
O
O
O
O
O
O
Het
N
N
n
Cl
Br
F3C
N
H2N
Cl
N
H
N
O
N
H2N
Cl
H2N
Cl
H
H
H
N
N
N
N
16a
16b
16c
12
13
14
15
Figure 2. Structures of the lone 3-aminopicolinamide mGlu4 PAM (7), and a diverse
array of inactive functionalized picolinamide head groups 8–15 (inset).
Scheme 1. Preparation of analogs 17. Reagents and conditions: (a) 3-aminopicolinic
acid or 3-hydroxypicolinic acid, HATU, DIEA, DCM:DMF, rt, 24 h, 65–90%.17

R. D. Gogliotti et al. / Bioorg. Med. Chem. Lett. 26 (2016) 2915–2919
2917
Table 1
Structures and mGlu4 PAM activity of analogs 17
R
NH2
O
N
H
Cl
N
17
Compd
R
mGlu4 EC50
(l
M)a
pEC50 SEMa
7.02 0.50
% Glu Maxb
O
17a
0.095
89.1 3.9
63.2 1.8
60.7 2.2
N
N
∗
O
O
∗
17b
17c
2.19
5.66 0.07
6.04 0.09
O
0.921
N
N
∗
O
17d
0.689
6.16 0.14
122.5 6.2
∗
O
O
17e
17f
0.236
3.96
6.63 0.21
5.40 0.01
43.9 6.2
76.8 0.6
N
N
∗
O
∗
Cl
O
O
17g
17h
>10
>5
42.3 2.6
N
N
∗
O
0.319
6.50 0.07
71.7 11.1
∗
O
17i
17j
17k
17l
1.25
>10
>10
2.80
5.90 0.05
>5
68.9 0.8
39.6 4.7
12.7 3.0
66.2 1.4
N
N
N
N
N
∗
O
∗
O
>5
∗
O
5.55 0.07
∗
Cl
F
O
17m
17n
1.86
2.52
5.73 0.05
5.60 0.13
75.9 0.9
92.8 2.4
N
∗
O
N
N
∗
N
O
17o
17p
0.758
1.61
6.12 0.05
5.79 0.04
45.3 4.1
∗
O
74.5 2.7
N
∗
(continued on next page)

2918
R. D. Gogliotti et al. / Bioorg. Med. Chem. Lett. 26 (2016) 2915–2919
Table 1 (continued)
Compd
R
mGlu4 EC50
>10
(l
M)a
pEC50 SEMa
% Glu Maxb
13.8 3.3
O
17q
17r
>5
N
N
∗
O
1.28
5.89 0.08
52.0 3.5
∗
O
17s
17t
>10
>5
47.7 2.7
97.9 4.0
89.8 2.0
N
O
∗
∗
N
0.065
1.35
7.19 0.11
5.87 0.15
N
O
∗
N
17u
N
a
Calcium mobilization mGlu4 assay; values are average of n = 3.
b
Amplitude of response in the presence of 30 l
M test compound, normalized to a standard compound, PHCCC (100% Glu Max).11–16
PAM 17t (VU0483872), in the same paradigm, proved to be
more efficacious than 6 (Fig. 5), displaying a minimum effective
dose (MED) of 1 mg/kg p.o. and robust reversal at 3 mg/kg p.o.
comparable to candidate 6 at 10 mg/kg p.o. Once again, as our
previous PBL study was IV, we also collected plasma and brain
samples from the oral HIC study to assess PK/PD. In this case, total
brain levels reached 172 nM (Kp = 0.2), a value greater than
3.5-fold above the rat mGlu4 PAM EC50 (46.6 nM). Thus, both
3-aminopicolinamide derivatives proved to be potent mGlu4 PAMs
in vitro and in vivo.
In summary, we report the first detailed SAR of a novel series of
mGlu4 PAMs based on a 3-aminopicolinamide warhead. New
mGlu4 PAMs 17a (VU0477886) and 17t (VU0483872) proved to
be potent PAMs, possessed favorable physicochemical properties
and DMPK properties, displayed excellent CNS penetration and
demonstrated robust in vivo efficacy in the HIC preclinical model
of PD. Moreover, 17t performed as well, if not better than our first
mGlu4 PAM preclinical candidate 6 (VU0418506). While attractive
in many aspects, neither 17a nor 17t advanced as back-ups to 6
due to low Fu, suboptimal multispecies PK and poor projected
O
O
N
NH2
O
N
Cl
N
OH
O
N
H
Cl
O
N
N
H
N
19
18
, EC50 >10 μM
(44.2% Glu Max)
, EC50 = 125 nM
(115.4% Glu Max)
O
N
NH2
O
N
N
N
N
H
Cl
20
, EC50 = 296nM
(103.9% Glu Max)
Figure 3. Structures and mGlu4 PAM activities of close analogs of 17a and 17t,
highlighting the unique pharmacology of the 3-aminopicolinamide.
the oral HIC study to assess PK/PD. In this case, total brain levels
reached 334 nM (Kp = 0.3), a value greater than 2-fold above the
rat mGlu4 PAM EC50 (128 nM).
Figure 4. Reversal of haloperidol-induced catalepsy (HIC) with either 17a
(VU0477886) or preclinical candidate 6 (VU0418506). Dosed orally as a microsus-
pension in 0.1% Tween80/0.5% methylcellulose bead-milled 30 min after haloperi-
dol (1.5 mg/kg). n = 9–10 rats/group, *p <0.05 in comparison to vehicle.
Figure 5. Reversal of haloperidol-induced catalepsy (HIC) with either 17t
(VU0483872) or preclinical candidate 6 (VU0418506). Dosed orally as a microsus-
pension in 0.1% Tween80/0.5% methylcellulose bead-milled 30 min after haloperi-
dol (1.5 mg/kg). n = 9–10 rats/group, *p <0.05 in comparison to vehicle.

R. D. Gogliotti et al. / Bioorg. Med. Chem. Lett. 26 (2016) 2915–2919
2919
Morrison, R.; Daniels, J. S.; Weaver, C. D.; Conn, P. J.; Lindsley, C. W.; Niswender,
C. M.; Hopkins, C. R. J. Med. Chem. 2011, 54, 7639.
14. Engers, D. W.; Niswender, C. M.; Weaver, C. D.; Jadhav, S.; Menon, U. N.;
Zamorano, R.; Conn, P. J.; Lindsley, C. W.; Hopkins, C. R. J. Med. Chem. 2009, 52,
4115.
15. Jones, C. K.; Bubser, M.; Thompson, A. D.; Dickerson, J. W.; Turle-Lorenzo, N.;
Amalric, M.; Blobaum, A. L.; Bridges, T. M.; Morrison, R. D.; Jadhav, S.; Engers, D.
W.; Italiano, K.; Bode, J.; Daniels, J. S.; Lindsley, C. W.; Hopkins, C. R.; Conn, P. J.;
Niswender, C. M. J. Pharmacol. Exp. Ther. 2012, 340, 404.
human PK. However, both represent new in vivo tool compounds
to study mGlu4 potentiation, and demonstrate solid PK/PD
relationships in HIC. Efforts towards suitable back-up compounds
continue and will be reported in due course.
Acknowledgments
16. Engers, D. W.; Blobaum, A. L.; Gogliotti, R. D.; Cheng, Y. -Y.; Salovich, J. M.;
Garcia-Barrantes, P.; Daniels, J. S.; Morrison, R. D.; Jones, C. K.; Soars. M. G.;
Zhou, X.; Hurely, J.; Macor, J. E.; Bronson, J. J.; Conn, P. J.; Lindsley, C. W.;
Niswender, C. M.; Hopkins, C. R. ACS Chem. Neurosci. in press.
This work was generously supported by the Michael J. Fox
Foundation (MJFF, LEAPS Award). Dr. Lindsley acknowledges the
Warren Family and Foundation for funding the William K. Warren,
Jr. Chair in Medicine. P.M.G. would like to acknowledge the VISP
program for its support.
17. Representative synthesis of 17a (VU0477886). N-(3-chloro-4-(1,3-
dioxoisoindolin-2-yl)phenyl)-3-aminopicolinamide. In
a
vial, 300 mg
(0.993 mmol, 1.0 equiv) of 2-(2-chloro-4-nitrophenyl)isoindoline-1,3-dione
were resuspended in dioxane. The suspension was cold in an ice bath and
purged with argon.
A previously prepared solution of tin(II) chloride
References and notes
(4.5 equiv) in concentrated hydrochloric acid (5 M concentration of SnCl2)
was added dropwise to the suspension. After 2 h of stirring at room
temperature, the reaction was neutralized carefully with aqueous potassium
carbonate 20%, filtered and extracted with diethyl ether. The organic phase was
dried with magnesium sulphate, filtered and the volatiles eliminated in vacuo
to yield a yellow solid (196 mg, 72%). 1H NMR (400.1 MHz, DMSO-d6) d (ppm):
7.97 (2H, m), 7.90 (2H, m), 7.14 (1H, d, J = 8.5 Hz), 6.76 (1H, d, J = 2.4 Hz), 6.60
(1H, dd, J = 8.6 Hz, J = 2.4 Hz), 5.74 (2H, s, –NH2).13C NMR (100.6 MHz, DMSO-
d6) d (ppm): 167.5, 151.5, 135.3, 132.7, 131.78, 131.76, 123.9, 116.5, 113.6,
113.0. In a vial, 0.088 mmol (1.2 equiv) of the 3-aminopicolinic acid were
added and dissolved in 0.5 mL mixture of DCM:DIEA (9:1), then 41 mg
(0.110 mmol, 1.5 equiv) of HATU were added. The mixture was stirred for
10 min, and 20 mg (0.073 mmol, 1.0 equiv) N-(4-aminophenyl)phthalimide
dissolved in 0.5 mL of DCM:DIEA (9:1), followed by 3 drops of DMF. The
reaction was stirred for 24 h at room temperature. After this time, the reaction
was quenched with the addition of water, and was worked up by extraction
with DCM (2 mL, thrice). The organic phased was filtered through a phase
separator, volatiles were evaporated, the crude was dissolved in DMSO and
purified by preparative HPLC. Cream powder. 1H NMR (400.1 MHz, CDCl3) d
(ppm): 10.33 (1H, s), 8.16 (1H, d, J = 2.3 Hz), 8.01 (2H, m), 7.95 (1H, dd,
J = 4.2 Hz, J = 1.1 Hz), 7.83 (2H, m), 7.74 (1H, dd, J = 8.6 Hz, J = 2.3 Hz), 7.35 (1H,
d, J = 8.6 Hz), 7.25 (1H, dd, J = 8.4 Hz, J = 4.3 Hz), 7.09 (1H, dd, J = 8.4 Hz,
J = 1.2 Hz). 13C NMR (100.6 MHz, CDCl3) d (ppm): 166.8, 165.6, 146.3, 139.9,
136.6, 134.4, 133.6, 131.9, 130.7, 128.6, 127.9, 125.4, 124.4, 120.6, 118.3. HRMS
(TOF, ES+) C20H14ClN4O3 [M+H]+ calcd mass 393.0754, found 394.0753.
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