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1.  Is There a Path Forward for mGlu2 Positive Allosteric Modulators for the Treatment of Schizophrenia? 
ACS Chemical Neuroscience  2013;4(2):211-213.
Two recent Phase II results show opposing outcomes for the potential of activators of mGlu2 in the treatment of schizophrenia. The first outcome revealed that Eli Lilly’s mGlu2/3 agonist, pomaglumetad methionil (LY2140023), failed to meet the primary efficacy end point. The second report showed the mGlu2 positive allosteric modulator (PAM) from Addex (ADX71149) in conjunction with Janssen Research & Development met the primary objectives of safety, tolerability and demonstrated an effect on negative symptoms in patients.
PMCID: PMC3582287  PMID: 23421671
Agonist; mGlu2/3; mGlu2; positive allosteric modulator; PAM; Phase II
2.  Synthesis of 2,3-diarylsubstituted indazoles utilizing a Suzuki cross-coupling/deprotection/N-arylation sequence 
Tetrahedron letters  2010;51(29):3796-3799.
Herein we report a general synthesis of 1,3-diarylsubstituted indazoles utilizing a two-step Suzuki cross-coupling/deprotection/N-arylation sequence. This procedure proceeds in excellent overall yield starting from the 3-iodo-N-Boc indazole derivative allowing for rapid access to these compounds.
PMCID: PMC2893583  PMID: 20606711
3.  Re-exploration of the PHCCC Scaffold: Discovery of Improved Positive Allosteric Modulators of mGluR4 
ACS chemical neuroscience  2010;1(6):411-419.
This Letter describes a detailed SAR analysis of the mGluR4 positive allosteric modulator, PHCCC. We have now developed compounds with improved potency and efficacy; in addition, compounds are presented that show selectivity for mGluR4 versus the other mGluR subtypes.
PMCID: PMC2889702  PMID: 20582156
metabotropic glutamate receptor 4; allosteric modulation; positive allosteric modulator; PHCCC; Parkinson's disease; structure-activity relationship; SAR
4.  Inhibition of the TRPC5 ion channel protects the kidney filter 
The Journal of Clinical Investigation  2013;123(12):5298-5309.
An intact kidney filter is vital to retention of essential proteins in the blood and removal of waste from the body. Damage to the filtration barrier results in albumin loss in the urine, a hallmark of cardiovascular disease and kidney failure. Here we found that the ion channel TRPC5 mediates filtration barrier injury. Using Trpc5-KO mice, a small-molecule inhibitor of TRPC5, Ca2+ imaging in isolated kidney glomeruli, and live imagining of podocyte actin dynamics, we determined that loss of TRPC5 or its inhibition abrogates podocyte cytoskeletal remodeling. Inhibition or loss of TRPC5 prevented activation of the small GTP-binding protein Rac1 and stabilized synaptopodin. Importantly, genetic deletion or pharmacologic inhibition of TRPC5 protected mice from albuminuria. These data reveal that the Ca2+-permeable channel TRPC5 is an important determinant of albuminuria and identify TRPC5 inhibition as a therapeutic strategy for the prevention or treatment of proteinuric kidney disease.
PMCID: PMC3859394  PMID: 24231357
5.  mGluR4-positive allosteric modulation as potential treatment for Parkinson’s disease 
Future medicinal chemistry  2009;1(3):501-513.
Although Parkinson’s disease was first diagnosed nearly 200 years ago, its effective treatment still remains elusive for most of those diagnosed. The gold standard of treatment for most patients is 3,4-dihydroxy-l-phenylalanine. This drug works for most individuals early in the disease; however, resistant symptoms start to emerge after several years of treatment. There has been increased interest in finding novel therapies to help Parkinson’s disease patients. Such strategies may have the benefit of not only treating the symptomatic issues of the disorder, but might also offer promise in protecting dopaminergic neurons from further degeneration. One such target that is now receiving much attention from the scientific community is the metabotropic glutamate receptor mGluR4. In this article, we briefly review Parkinson’s disease and then recent work in the mGluR area, with a focus on the efforts being made toward finding and optimizing novel mGluR4 positive allosteric modulators (PAMs). Preclinically in rodent models, mGluR4 activation has offered much promise as a novel treatment of Parkinson’s disease. Additionally, the specific use of PAMs, rather than direct-acting agonists at the orthosteric glutamate site, continues to be validated as a viable treatment option for this target. It is anticipated that continued progress in this area will further our understanding of the potential of mGluR4 modulation as a novel symptomatic and potentially disease-modifying treatment for Parkinson’s disease.
PMCID: PMC2790174  PMID: 20161443
6.  "Molecular Switches" on mGluR Allosteric Ligands That Modulate Modes of Pharmacology 
Biochemistry  2011;50(13):2403-2410.
G-Protein-coupled receptors (GPCRs) represent the largest class of drug targets, accounting for more than 40% of marketed drugs; however, discovery efforts for many GPCRs have failed to provide viable drug candidates. Historically, drug discovery efforts have focused on developing ligands that act at the orthosteric site of the endogenous agonist. Recently, efforts have focused on functional assay paradigms and the discovery of ligands that act at allosteric sites to modulate receptor function in either a positive, negative, or neutral manner. Allosteric modulators have numerous advantages over orthosteric ligands, including high subtype selectivity; the ability to mimic physiological conditions; the lack of densensitization, downregulation, and internalization; and reduced side effects. Despite these virtues, challenging issues have now arisen for allosteric modulators of metabotropic glutamate receptors (mGluRs): shallow SAR, ligand-directed trafficking, and the identification of subtle “molecular switches” that modulate the modes of pharmacology. Here, we will discuss the impact of modest structural changes to multiple mGluR allosteric ligands scaffolds that unexpectedly modulate pharmacology and raise concerns over metabolism and the pharmacology of metabolites.
PMCID: PMC3792571  PMID: 21341760
7.  ACS Chemical Neuroscience Molecule Spotlight on Suvorexant 
ACS Chemical Neuroscience  2012;3(9):647-648.
Suvorexant is a dual orexin antagonist currently in Phase III clinical trials for the modulation of sleep and is being developed by Merck. Recent Phase III results showed that patients taking the drug fell asleep faster and slept longer than those on placebo.
PMCID: PMC3447389  PMID: 23024835
Sleep; insomnia; novel mechanism; orexin antagonist; bioavailability (F)
8.  Iterative experimental and virtual high-throughput screening identifies metabotropic glutamate receptor subtype 4 positive allosteric modulators 
Journal of molecular modeling  2012;18(9):4437-4446.
Activation of metabotropic glutamate receptor subtype 4 has been shown to be efficacious in rodent models of Parkinson’s disease. Artificial neural networks were trained based on a recently reported high throughput screen which identified 434 positive allosteric modulators of metabotropic glutamate receptor subtype 4 out of a set of approximately 155,000 compounds. A jury system containing three artificial neural networks achieved a theoretical enrichment of 15.4 when selecting the top 2% compounds of an independent test dataset. The model was used to screen an external commercial database of approximately 450,000 drug-like compounds. 1,100 predicted active small molecules were tested experimentally using two distinct assays of mGlu4 activity. This experiment yielded 67 positive allosteric modulators of metabotropic glutamate receptor subtype 4 that confirmed in both experimental systems. Compared to the 0.3% active compounds in the primary screen, this constituted an enrichment of 22 fold.
PMCID: PMC3766737  PMID: 22592386
Metabotropic glutamate receptor subtype 4; Virtual high-throughput screening; Machine learning; Quantitative structure-activity relationship; Enrichment
9.  ACS Chemical Neuroscience Molecule Spotlight on Potiga (Ezogabine) 
ACS Chemical Neuroscience  2012;3(8):632.
On June 10th, 2011, the U.S. Food and Drug Administration approved Potiga (ezogabine) as an add-on medication for the treatment of seizures in adults, and it is being developed by Valeant Pharmaceuticals.
PMCID: PMC3419453  PMID: 22896808
epilepsy; seizures; potassium channel opener; Kv7
10.  Discovery of a Series of 2-phenyl-N-(2-(pyrrolidin-1-yl)phenyl)acetamides as Novel Molecular Switches that Modulate Modes of Kv7.2 (KCNQ2) Channel Pharmacology: Identification of (S)-2-phenyl-N-(2-(pyrrolidin-1-yl)phenyl)butanamide (ML252) as a Potent, Brain Penetrant Kv7.2 Channel Inhibitor 
Journal of medicinal chemistry  2012;55(15):6975-6979.
A potent and selective inhibitor of KCNQ2, (S)-5 (ML252, IC50 = 69 nM), was discovered after a high-throughput screen of the MLPCN library was performed. SAR studies revealed a small structural change (ethyl group to hydrogen) caused a functional shift from antagonist to agonist activity (37, EC50 = 170 nM), suggesting an interaction at a critical site for controlling gating of KCNQ2 channels.
PMCID: PMC3530927  PMID: 22793372
KCNQ2; inhibitor; Kv7; ion channels; ML252; MLPCN probe; mode switch; CNS
11.  DMH1, a Highly Selective Small Molecule BMP Inhibitor Promotes Neurogenesis of hiPSCs: Comparison of PAX6 and SOX1 Expression during Neural Induction 
ACS Chemical Neuroscience  2012;3(6):482-491.
Recent successes in deriving human-induced pluripotent stem cells (hiPSCs) allow for the possibility of studying human neurons derived from patients with neurological diseases. Concomitant inhibition of the BMP and TGF-β1 branches of the TGF-β signaling pathways by the endogenous antagonist, Noggin, and the small molecule SB431542, respectively, induces efficient neuralization of hiPSCs, a method known as dual-SMAD inhibition. The use of small molecule inhibitors instead of their endogenous counterparts has several advantages including lower cost, consistent activity, and the maintenance of xeno-free culture conditions. We tested the efficacy of DMH1, a highly selective small molecule BMP-inhibitor for its potential to replace Noggin in the neuralization of hiPSCs. We compare Noggin and DMH1-induced neuralization of hiPSCs by measuring protein and mRNA levels of pluripotency and neural precursor markers over a period of seven days. The regulation of five of the six markers assessed was indistinguishable in the presence of concentrations of Noggin or DMH1 that have been shown to effectively inhibit BMP signaling in other systems. We observed that by varying the DMH1 or Noggin concentration, we could selectively modulate the number of SOX1 expressing cells, whereas PAX6, another neural precursor marker, remained the same. The level and timing of SOX1 expression have been shown to affect neural induction as well as neural lineage. Our observations, therefore, suggest that BMP-inhibitor concentrations need to be carefully monitored to ensure appropriate expression levels of all transcription factors necessary for the induction of a particular neuronal lineage. We further demonstrate that DMH1-induced neural progenitors can be differentiated into β3-tubulin expressing neurons, a subset of which also express tyrosine hydroxylase. Thus, the combined use of DMH1, a highly specific BMP-pathway inhibitor, and SB431542, a TGF-β1-pathway specific inhibitor, provides us with the tools to independently regulate these two pathways through the exclusive use of small molecule inhibitors.
PMCID: PMC3400384  PMID: 22860217
Induced pluripotent stem cells; iPS; neural induction; neural differentiation; TGF-β; transcription factors
12.  Eliciting Renal Failure in Mosquitoes with a Small-Molecule Inhibitor of Inward-Rectifying Potassium Channels 
PLoS ONE  2013;8(5):e64905.
Mosquito-borne diseases such as malaria and dengue fever take a large toll on global health. The primary chemical agents used for controlling mosquitoes are insecticides that target the nervous system. However, the emergence of resistance in mosquito populations is reducing the efficacy of available insecticides. The development of new insecticides is therefore urgent. Here we show that VU573, a small-molecule inhibitor of mammalian inward-rectifying potassium (Kir) channels, inhibits a Kir channel cloned from the renal (Malpighian) tubules of Aedes aegypti (AeKir1). Injection of VU573 into the hemolymph of adult female mosquitoes (Ae. aegypti) disrupts the production and excretion of urine in a manner consistent with channel block of AeKir1 and renders the mosquitoes incapacitated (flightless or dead) within 24 hours. Moreover, the toxicity of VU573 in mosquitoes (Ae. aegypti) is exacerbated when hemolymph potassium levels are elevated, suggesting that Kir channels are essential for maintenance of whole-animal potassium homeostasis. Our study demonstrates that renal failure is a promising mechanism of action for killing mosquitoes, and motivates the discovery of selective small-molecule inhibitors of mosquito Kir channels for use as insecticides.
PMCID: PMC3666979  PMID: 23734226
13.  ACS Chemical Neuroscience Molecule Spotlight on BMS-708163 
ACS Chemical Neuroscience  2012;3(3):149-150.
BMS-708163 is a novel, sulfonamide containing γ-secretase inhibitor from Bristol-Myers Squibb Co. currently in Phase II clinical trials for the treatment of Alzheimer’s disease (AD).
PMCID: PMC3369796  PMID: 22860183
Alzheimer's disease; amyloid hypothesis; gamma-secretase inhibitors; GSI
14.  Allosteric Modulation of 7 Transmembrane Spanning Receptors: Theory, Practice and Opportunities for CNS Drug Discovery1 
Journal of Medicinal Chemistry  2012;55(4):1445-1464.
PMCID: PMC3349997  PMID: 22148748
G Protein-Coupled Receptor; Seven Transmembrane Receptor; allosteric; positive allosteric modulator; negative allosteric modulator; silent allosteric modulator; ago-potentiator; partial antagonist; molecular switch; ligand-biased signaling
15.  ACS Chemical Neuroscience Molecule Spotlight on Begacestat (GSI-953) 
ACS Chemical Neuroscience  2012;3(1):3-4.
A “second generation” γ-secretase, Begacestat (GSI-953), which is more selective against Notch-signaling, has shown promise in recent Phase I clinical trials. Begacestat, a novel, 2,5-disubsitituted thiophene sulfonamide from Wyeth (now Pfizer) is under evaluation for the treatment of Alzheimer’s disease.
PMCID: PMC3369785  PMID: 22860177
Alzheimer's disease, γ-secretase inhibitors, GSI, Aβ-peptides
16.  The Discovery and Characterization of ML218: A Novel, Centrally Active T-Type Calcium Channel Inhibitor with Robust Effects in STN Neurons and in a Rodent Model of Parkinson’s Disease 
ACS Chemical Neuroscience  2011;2(12):730-742.
T-Type Ca2+ channel inhibitors hold tremendous therapeutic potential for the treatment of pain, epilepsy, sleep disorders, essential tremor, and other neurological disorders; however, a lack of truly selective tools has hindered basic research, and selective tools from the pharmaceutical industry are potentially burdened with intellectual property (IP) constraints. Thus, an MLPCN high-throughput screen (HTS) was conducted to identify novel T-type Ca2+ channel inhibitors free from IP constraints, and freely available through the MLPCN, for use by the biomedical community to study T-type Ca2+ channels. While the HTS provided numerous hits, these compounds could not be optimized to the required level of potency to be appropriate tool compounds. Therefore, a scaffold hopping approach, guided by SurflexSim, ultimately afforded ML218 (CID 45115620), a selective T-type Ca2+ (Cav3.1, Cav3.2, Cav3.3) inhibitor (Cav3.2, IC50 = 150 nM in Ca2+ flux; Cav3.2 IC50 = 310 nM; and Cav3.3 IC50 = 270 nM, respectively in patch clamp electrophysiology) with good DMPK properties, acceptable in vivo rat PK, and excellent brain levels. Electrophysiology studies in subthalamic nucleus (STN) neurons demonstrated robust effects of ML218 on the inhibition of T-type calcium current, inhibition of low threshold spike, and rebound burst activity. Based on the basal ganglia circuitry in Parkinson’s disease (PD), the effects of ML218 in STN neurons suggest a therapeutic role for T-type Ca2+ channel inhibitors, and ML218 was found to be orally efficacious in haloperidol-induced catalepsy, a preclinical PD model, with comparable efficacy to an A2A antagonist, a clinically validated PD target. ML218 proves to be a powerful new probe to study T-type Ca2+ function in vitro and in vivo, and freely available.
PMCID: PMC3285241  PMID: 22368764
T-Type calcium channel; inhibitor; electrophysiology; Parkinson’s disease
17.  ACS Chemical Neuroscience Molecule Spotlight on RG1678 
ACS Chemical Neuroscience  2011;2(12):685-686.
RG1678 is a glycine transporter-1 inhibitor currently in Phase III trials for the treatment of the negative symptoms of schizophrenia and is being developed by Roche (in combination with Chugai). Recent Phase II data shows that RG1678 is effective in reducing the negative symptoms when given in combination with second generation antipsychotics.
PMCID: PMC3369722  PMID: 22860161
Schizophrenia; negative symptoms; RG1678; glycine transporter-1 inhibitor; GlyT1
18.  Synthesis and SAR of a novel metabotropic glutamate receptor 4 (mGlu4) antagonist: Unexpected ‘molecular switch’ from a closely related mGlu4 positive allosteric modulator 
Herein we report the discovery and SAR of a novel antagonist of metabotropic glutamate receptor 4 (mGlu4). The antagonist was discovered via a molecular switch from a closely related mGlu4 positive allosteric modulator (PAM). This antagonist (VU0448383) displays an IC50 value of 8.2 ± 0.4 μM and inhibits an EC80 glutamate response by 63.1 ± 6.6%.
PMCID: PMC3319082  PMID: 22030026
Metabotropic glutamate receptor 4; mGlu4; Molecular switch; Antagonist
19.  ACS Chemical Neuroscience Molecule Spotlight on Viibryd (Vilazodone) 
ACS Chemical Neuroscience  2011;2(10):554.
On January 21, 2011, the U.S. Food and Drug Administration approved Viibryd, a new selective serotonin reuptake inhibitor (SSRI), to treat major depressive disorder in adults developed by Clinical Data, Inc.
PMCID: PMC3369713  PMID: 22860155
Depression; major depressive disorder; antidepressant; SSRI
20.  Discovery, Synthesis, and Structure–Activity Relationship of a Series of N-Aryl-bicyclo[2.2.1]heptane-2-carboxamides: Characterization of ML213 as a Novel KCNQ2 and KCNQ4 Potassium Channel Opener 
ACS Chemical Neuroscience  2011;2(10):572-577.
Herein we report the discovery, synthesis, and evaluation of a series of N-aryl-bicyclo[2.2.1]heptane-2-carboxamides as selective KCNQ2 (Kv7.2) and KCNQ4 (Kv7.4) channel openers. The best compound, 1 (ML213), has an EC50 of 230 nM (KCNQ2) and 510 nM (KCNQ4) and is selective for KCNQ2 and KCNQ4 channels versus a large battery of related potassium channels, as well as affording modest brain levels. This represents the first report of unique selectivity profiles for KCNQ2 and KCNQ4 over the other channels (KCNQ1/3/5) and as such should prove to be a valuable tool compound for understanding these channels in regulating neuronal activity.
PMCID: PMC3223964  PMID: 22125664
KCNQ2; KCNQ4; activator; Kv7; ion channels; ML218; MLPCN probe
21.  Discovery, Synthesis, and Structure Activity Relationship of a Series of N-Aryl- bicyclo[2.2.1]heptane-2-carboxamides: Characterization of ML213 as a Novel KCNQ2 and KCNQ4 Potassium Channel Opener 
ACS chemical neuroscience  2011;2(10):572-577.
Herein we report the discovery, synthesis and evaluation of a series of N-Aryl-bicyclo[2.2.1]heptane-2-carboxamides as selective KCNQ2 (Kv7.2) and KCNQ4 (Kv7.4) channel openers. The best compound, 1 (ML213) has an EC50 of 230 nM (KCNQ2) and 510 nM (KCNQ4) and is selective for KCNQ2 and KCNQ4 channels versus a large battery of related potassium channels, as well as affording modest brain levels. This represents the first report of unique selectivity profile for KCNQ2 and KCNQ4 over the other channels (KCNQ1/3/5) and as such should prove to be a valuable tool compound for understanding these channels in regulating neuronal activity.
PMCID: PMC3223964  PMID: 22125664
22.  Application of Small Organic Molecules Reveals Cooperative TGFβ and BMP Regulation of Mesothelial Cell Behaviors 
ACS chemical biology  2011;6(9):952-961.
Epicardial development is a process during which epithelial sheet movement, single cell migration and differentiation are coordinated to generate coronary arteries. Signaling cascades regulate the concurrent and complex nature of these three events. Through simple and highly reproducible assays, we identified small organic molecules that impact signaling pathways regulating these epicardial behaviors. Subsequent biochemical analyses confirmed the specificity of these reagents and revealed novel targets for the widely used Dorsomorphin (DM) and LDN-193189 molecules. Using these newly characterized reagents, we show the broad regulation of epicardial cell differentiation, sheet movement and single cell migration by Transforming Growth Factor β (TGFβ). With the DM analog, DMH1, a highly specific Bone Morphogenetic Protein (BMP) inhibitor, we demonstrate the cooperative yet exclusive role for BMP signaling in regulation of sheet migration. The action of DMH1 reveals that small organic molecules (SOM) can intervene on a single epicardial behavior while leaving other concurrent behaviors intact. All SOM data were confirmed by reciprocal experiments using growth factor addition and/or application of established non-SOM inhibitors. These compounds can be applied to cell lines or native proepicardial tissue. Taken together, these data establish the efficacy of chemical intervention for analysis of epicardial behaviors and provide novel reagents for analysis of epicardial development and repair.
PMCID: PMC3177035  PMID: 21740033
23.  Selective inhibition of the Kir2 family of inward rectifier potassium channels by a small molecule probe: the discovery, SAR and pharmacological characterization of ML133 
ACS chemical biology  2011;6(8):845-856.
The Kir inward rectifying potassium channels have a broad tissue distribution and are implicated in a variety of functional roles. At least seven classes (Kir1 – Kir7) of structurally related inward rectifier potassium channels are known, and there are no selective small molecule tools to study their function. In an effort to develop selective Kir2.1 inhibitors, we performed a high-throughput screen (HTS) of more than 300,000 small molecules within the MLPCN for modulators of Kir2.1 function. Here we report one potent Kir2.1 inhibitor, ML133, which inhibits Kir2.1 with IC50 of 1.8 μM at pH 7.4 and 290 nM at pH 8.5, but exhibits little selectivity against other members of Kir2.x family channels. However, ML133 has no effect on Kir1.1 (IC50 > 300 μM), and displays weak activity for Kir4.1 (76 μM) and Kir7.1 (33 μM), making ML133 the most selective small molecule inhibitor of the Kir family reported to date. Due to the high homology within the Kir family, the channels share a common design of a pore region flanked by two transmembrane domains, identification of site(s) critical for isoform specificity would be an important basis for future development of more specific and potent Kir inhibitors. Using chimeric channels between Kir2.1 and Kir1.1 and site-directed mutagenesis, we have identified D172 and I176 within M2 segment of Kir2.1 as molecular determinants critical for the potency of ML133 mediated inhibition. Double mutation of the corresponding residues of Kir1.1 to those of Kir2.1 (N171D and C175I) transplants ML133 inhibition to Kir1.1. Together, the combination of a potent, Kir2 family selective inhibitor and identification of molecular determinants for the specificity provides both a tool and a model system to enable further mechanistic studies of modulation of Kir2 inward rectifier potassium channels.
PMCID: PMC3177608  PMID: 21615117
Kir2.1; inward rectifying potassium channel; ion channel; mutagenesis; structure-activity-relationship; medicinal chemistry; ion works; patch clamp; high throughput screening; MLPCN
24.  Recent Progress on the Identification of Metabotropic Glutamate 4 Receptor Ligands and Their Potential Utility as CNS Therapeutics 
ACS Chemical Neuroscience  2011;2(8):433-449.
This Review describes recent activity in the advancement of ligands for the metabotropic glutamate 4 receptor subtype and their potential utility as central nervous system (CNS) therapeutics. Until recently, there was a paucity of compounds with suitable selectivity and druglike properties to elucidate the value of this target. The search for selective entities has led several groups to the investigation of allosteric modulators as a path to optimization of potential ligands. Recent efforts, discussed here, have afforded a variety of derivatives with improvements in potency, solubility, and pharmacokinetic properties that garner support for continued investigation and optimization.
PMCID: PMC3369748  PMID: 22860170
Metabotropic glutamate receptor 4; orthosteric ligand; allosteric modulator; Parkinson’s disease; anxiety; pain; cognitive disorders; psychiatric disorders; neurodegenerative disorders; Class C GPCR
25.  ACS Chemical Neuroscience Molecule Spotlight on STX209 (Arbaclofen) 
ACS Chemical Neuroscience  2011;2(8):381.
STX209 (arbaclofen) is a γ-amino butyric acid type B (GABAB) receptor agonist from Seaside Therapeutics currently in clinical trials for autism spectrum disorders (ASD). The company has initiated a phase 2b study after positive results from a phase 2a trial, announced September 2010 ( Trial_Initiation%206%2021%202011%20Final.pdf).
PMCID: PMC3369760  PMID: 22860166
STX209; autism spectrum disorder (ASD); GABA

Results 1-25 (55)