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Published: 10 March 2023

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1

Panch, Sandhya R., Michael Bozik, Thomas Brown, Ulrike Demarco, Jamie Hahn, Alexander Komarov, Tamika Magee, et al. "Dexpramipexole As a Steroid-Sparing Agent in Hypereosinophilic Syndromes (HES): An Open-Label Proof-of-Concept Study." Blood 128, no. 22 (December 2, 2016): 1327. http://dx.doi.org/10.1182/blood.v128.22.1327.1327.

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Abstract Hypereosinophilic syndromes (HES) are a heterogeneous group of disorders characterized by peripheral eosinophilia and eosinophil-related end organ damage. Whereas most patients respond to steroid therapy, high doses are often necessary and serious side effects are common. Dexpramipexole (KNS-760704) is an orally bioavailable synthetic amino-benzothiazole that was in development for the treatment of amyotrophic lateral sclerosis (ALS). Despite failure to meet the primary efficacy endpoint in a phase 3 trial in ALS patients, dexpramipexole showed an excellent safety profile and was found to significantly decrease absolute eosinophil counts (AEC) in >70% of the study participants. Consequently, a proof-of-concept study was designed to evaluate the safety and efficacy of dexpramipexole as a steroid-sparing agent in 10 HES subjects. Subjects with HES on steroid monotherapy were eligible for the study if they required ≥10 mg prednisone or equivalent for control of symptoms and eosinophilia. Subjects with AEC <1000/uL and no active symptoms entered a lead-in period, consisting of a standardized steroid taper with weekly assessment of AEC and symptoms to establish a "minimally effective corticosteroid dose (MECD)". Those with AEC ≥1000/uL entered directly into the treatment phase. Once the MECD was established, treatment with dexpramipexole (150 mg twice daily) was initiated. After 12 weeks of treatment, a standardized corticosteroid taper was attempted to determine the "MECD on dexpramipexole". Clinical assessments, including bone marrow and tissue biopsies of affected organs (when possible), were performed prior to and after 12 weeks of dexpramipexole. The primary efficacy endpoint was defined as a ≥50 % change in prednisone dose to maintain AEC at or below baseline levels and control clinical symptoms. Study enrollment is complete. Median age at enrollment was 51 years (22-72) with 40% women. Baseline clinical manifestations included eosinophilic gastrointestinal disease (60%), pulmonary involvement (50%), skin, muscle, sinus, and cardiac disease. Median baseline AEC was 670/uL (280-2540) and median MECD at baseline was 18.75 mg of prednisone (10-25). To date, the MECD on dexpramipexole has been determined for 7 subjects, and 3 subjects continue on study and have not completed the steroid taper on dexpramipexole. Two of the 7 evaluable subjects met the primary end point. Both subjects reached a MECD of 0 mg of prednisone and had complete symptom resolution with AEC of 0/uL within 3 months of initiating treatment with dexpramipexole. They remain in clinical remission on dexpramipexole monotherapy for 7 and 12 months, respectively. One additional subject who did not meet the primary endpoint at 3 months, was able to maintain a stable dose of 12.5 mg of prednisone with clinical improvement. She has remained on dexpramipexole and has demonstrated a delayed response with AEC 100/uL on 8.75 mg prednisone (50% of her baseline MECD) at 6 months. The remaining 4 evaluable subjects failed to respond and were taken off study. No deaths or drug related adverse events were observed, although 2 subjects reported transient palpitations and insomnia that resolved without drug discontinuation. Bone marrow biopsies performed at 12 weeks revealed markedly decreased AEC and basophils in responders as compared to baseline samples, and residual eosinophils appeared left-shifted. Other cell lineages were unchanged. Gastrointestinal biopsies in 1 responder demonstrated complete resolution of tissue eosinophilia after 5 months on dexpramipexole. Flow cytometry demonstrated no difference in CD34+ or CD34+IL-5R+ cell numbers after 12 weeks of treatment, but a decrease in eosinophil expression of Siglec 8, an inhibitory receptor expressed only on mature eosinophils. These changes were not observed in the non-responders. CD34+ cell cultures using normal cord blood samples also suggest a delay in maturation of the eosinophil lineage in the presence of dexpramipexole. Given the frequency of steroid-induced morbidity in patients with HES, alternate therapeutic options are critical. In this pilot study, dexpramipexole showed remarkable efficacy as a steroid-sparing agent without apparent toxicity in a subset of subjects with steroid-responsive HES. Although the mechanism of action is unknown, preliminary data suggest that dexpramipexole may affect eosinophil maturation in the bone marrow. Disclosures Bozik: Knopp Biosciences: Employment. Brown:Leidos Biomedical Research Inc.: Employment. Demarco:Knopp Biosciences: Employment. Komarov:Knopp Biosciences: Employment. Magee:Leidos Biomedical Research Inc.: Employment. Prussin:Knopp Biosciences: Employment. Signore:Knopp Biosciences: Employment. Sullivan:Knopp Biosciences: Employment. Wetzler:Leidos Biomedical Research Inc.: Employment. Dunbar:Novartis: Research Funding. Dworetzky:Knopp Biosciences: Employment.
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2

Panch, Sandhya R., Michael E. Bozik, Thomas Brown, Michelle Makiya, Calman Prussin, Donald G. Archibald, Gregory T. Hebrank, et al. "Dexpramipexole as an oral steroid-sparing agent in hypereosinophilic syndromes." Blood 132, no. 5 (August 2, 2018): 501–9. http://dx.doi.org/10.1182/blood-2018-02-835330.

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Key Points GC-sparing treatment alternatives are a critical need for patients with HESs. The orally bioactive drug dexpramipexole demonstrated clinical efficacy with an excellent safety profile in a subset of patients with HESs.
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3

Gleich, Gerald J. "Dexpramipexole: a new antieosinophil drug?" Blood 132, no. 5 (August 2, 2018): 461–62. http://dx.doi.org/10.1182/blood-2018-06-851600.

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4

Mignani, Serge, Jean-Pierre Majoral, Jean-François Desaphy, and Giovanni Lentini. "From Riluzole to Dexpramipexole via Substituted-Benzothiazole Derivatives for Amyotrophic Lateral Sclerosis Disease Treatment: Case Studies." Molecules 25, no. 15 (July 22, 2020): 3320. http://dx.doi.org/10.3390/molecules25153320.

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The 1,3-benzothiazole (BTZ) ring may offer a valid option for scaffold-hopping from indole derivatives. Several BTZs have clinically relevant roles, mainly as CNS medicines and diagnostic agents, with riluzole being one of the most famous examples. Riluzole is currently the only approved drug to treat amyotrophic lateral sclerosis (ALS) but its efficacy is marginal. Several clinical studies have demonstrated only limited improvements in survival, without benefits to motor function in patients with ALS. Despite significant clinical trial efforts to understand the genetic, epigenetic, and molecular pathways linked to ALS pathophysiology, therapeutic translation has remained disappointingly slow, probably due to the complexity and the heterogeneity of this disease. Many other drugs to tackle ALS have been tested for 20 years without any success. Dexpramipexole is a BTZ structural analog of riluzole and was a great hope for the treatment of ALS. In this review, as an interesting case study in the development of a new medicine to treat ALS, we present the strategy of the development of dexpramipexole, which was one of the most promising drugs against ALS.
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5

Kuang, Fei Li. "Dexpramipexole: A Potential Non-biologic Alternative for Patients with Eosinophilic Asthma?" US Respiratory & Pulmonary Diseases 7, no. 2 (2022): 36. http://dx.doi.org/10.17925/usrpd.2022.7.2.36.

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Dexpramipexole offers a potential non-biologic option for patients with eosinophilic asthma in that it lowers blood eosinophil count and improves lung function parameters. However, longer-term studies in patients treated by reducing blood or tissue eosinophils, whether through biologics or oral therapies, are needed to better understand the role of the eosinophil in human biology and disease pathogenesis and to better delineate the clinical efficacy of Dexpramizole in asthma.
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6

Muzzi, Mirko, Elisabetta Gerace, Daniela Buonvicino, Elisabetta Coppi, Francesco Resta, Laura Formentini, Riccardo Zecchi, et al. "Dexpramipexole improves bioenergetics and outcome in experimental stroke." British Journal of Pharmacology 175, no. 2 (May 12, 2017): 272–83. http://dx.doi.org/10.1111/bph.13790.

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7

Lequien, Valérie. "Le dexpramipexole, une piste prometteuse contre la SLA." Actualités Pharmaceutiques Hospitalières 6, no. 22 (May 2010): 9. http://dx.doi.org/10.1016/s1769-7344(10)70268-7.

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8

Kingwell, Katie. "Dexpramipexole shows promise for ALS in phase II trial." Nature Reviews Neurology 8, no. 1 (December 26, 2011): 4. http://dx.doi.org/10.1038/nrneurol.2011.204.

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9

Ludolph, Albert. "Dexpramipexol ist bei der Behandlung der ALS nicht wirksam." InFo Neurologie & Psychiatrie 15, no. 12 (December 2013): 32. http://dx.doi.org/10.1007/s15005-013-0696-z.

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10

Tang, Lu, Yun-peng Li, Juan Hu, Ai-hua Chen, and Yingli Mo. "Dexpramipexole attenuates myocardial ischemia/reperfusion injury through upregulation of mitophagy." European Journal of Pharmacology 899 (May 2021): 173962. http://dx.doi.org/10.1016/j.ejphar.2021.173962.

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11

Vieira, Fernando G., Eva LaDow, Andy Moreno, Joshua D. Kidd, Beth Levine, Kenneth Thompson, Alan Gill, Steven Finkbeiner, and Steven Perrin. "Dexpramipexole Is Ineffective in Two Models of ALS Related Neurodegeneration." PLoS ONE 9, no. 12 (December 19, 2014): e91608. http://dx.doi.org/10.1371/journal.pone.0091608.

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12

Coppi, Elisabetta, Daniele Lana, Federica Cherchi, Irene Fusco, Daniela Buonvicino, Matteo Urru, Giuseppe Ranieri, et al. "Dexpramipexole enhances hippocampal synaptic plasticity and memory in the rat." Neuropharmacology 143 (December 2018): 306–16. http://dx.doi.org/10.1016/j.neuropharm.2018.10.003.

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13

Muzzi, Mirko, Daniela Buonvicino, Matteo Urru, Lorenzo Tofani, and Alberto Chiarugi. "Repurposing of dexpramipexole to treatment of neonatal hypoxic/ischemic encephalopathy." Neuroscience Letters 687 (November 2018): 234–40. http://dx.doi.org/10.1016/j.neulet.2018.09.064.

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14

Dworetzky, Steven I., Gregory T. Hebrank, Donald G. Archibald, Ian J. Reynolds, Wildon Farwell, and Michael E. Bozik. "The targeted eosinophil-lowering effects of dexpramipexole in clinical studies." Blood Cells, Molecules, and Diseases 63 (March 2017): 62–65. http://dx.doi.org/10.1016/j.bcmd.2017.01.008.

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15

Alavian, Kambiz N., Steven I. Dworetzky, Laura Bonanni, Ping Zhang, Silvio Sacchetti, Maria A. Mariggio, Marco Onofrj, et al. "Effects of dexpramipexole on brain mitochondrial conductances and cellular bioenergetic efficiency." Brain Research 1446 (March 2012): 1–11. http://dx.doi.org/10.1016/j.brainres.2012.01.046.

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16

Lee, Seong-il, Janneke G. J. Hoeijmakers, Catharina G. Faber, Ingemar S. J. Merkies, Giuseppe Lauria, and Stephen G. Waxman. "The small fiber neuropathy NaV1.7 I228M mutation: impaired neurite integrity via bioenergetic and mitotoxic mechanisms, and protection by dexpramipexole." Journal of Neurophysiology 123, no. 2 (February 1, 2020): 645–57. http://dx.doi.org/10.1152/jn.00360.2019.

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Gain-of-function variants in voltage-gated sodium channel NaV1.7 that increase firing frequency and spontaneous firing of dorsal root ganglion (DRG) neurons have recently been identified in 5–10% of patients with idiopathic small fiber neuropathy (I-SFN). Our previous in vitro observations suggest that enhanced sodium channel activity can contribute to a decrease in length of peripheral sensory axons. We have hypothesized that sustained sodium influx due to the expression of SFN-associated sodium channel variants may trigger an energetic deficit in neurons that contributes to degeneration and loss of nerve fibers in SFN. Using an ATP FRET biosensor, we now demonstrate reduced steady-state levels of ATP and markedly faster ATP decay in response to membrane depolarization in cultured DRG neurons expressing an SFN-associated variant NaV1.7, I228M, compared with wild-type neurons. We also observed that I228M neurons show a significant reduction in mitochondrial density and size, indicating dysfunctional mitochondria and a reduced bioenergetic capacity. Finally, we report that exposure to dexpramipexole, a drug that improves mitochondrial energy metabolism, increases the neurite length of I228M-expressing neurons. Our data suggest that expression of gain-of-function variants of NaV1.7 can damage mitochondria and compromise cellular capacity for ATP production. The resulting bioenergetic crisis can consequently contribute to loss of axons in SFN. We suggest that, in addition to interventions that reduce ionic disturbance caused by mutant NaV1.7 channels, an alternative therapeutic strategy might target the bioenergetic burden and mitochondrial damage that occur in SFN associated with NaV1.7 gain-of-function mutations. NEW & NOTEWORTHY Sodium channel NaV1.7 mutations that increase dorsal root ganglion (DRG) neuron excitability have been identified in small fiber neuropathy (SFN). We demonstrate reduced steady-state ATP levels, faster depolarization-evoked ATP decay, and reduced mitochondrial density and size in cultured DRG neurons expressing SFN-associated variant NaV1.7 I228M. Dexpramipexole, which improves mitochondrial energy metabolism, has a protective effect. Because gain-of-function NaV1.7 variants can compromise bioenergetics, therapeutic strategies that target bioenergetic burden and mitochondrial damage merit study in SFN.
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17

Cudkowicz, Merit, Michael E. Bozik, Evan W. Ingersoll, Robert Miller, Hiroshi Mitsumoto, Jeremy Shefner, Dan H. Moore, et al. "The effects of dexpramipexole (KNS-760704) in individuals with amyotrophic lateral sclerosis." Nature Medicine 17, no. 12 (November 20, 2011): 1652–56. http://dx.doi.org/10.1038/nm.2579.

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18

Bozik, Michael E., James L. Mather, William G. Kramer, Valentin K. Gribkoff, and Evan W. Ingersoll. "Safety, Tolerability, and Pharmacokinetics of KNS-760704 (Dexpramipexole) in Healthy Adult Subjects." Journal of Clinical Pharmacology 51, no. 8 (August 2011): 1177–85. http://dx.doi.org/10.1177/0091270010379412.

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19

Talan, Jamie. "Encouraging Phase 2 Results for Dexpramipexole for ALS Prompt Phase 3 Trial." Neurology Today 11, no. 24 (December 2011): 9. http://dx.doi.org/10.1097/01.nt.0000410293.18909.d9.

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20

He, Ping, Doug Kerr, Thomas Marbury, Daniel Ries, Wildon Farwell, Scott Stecher, Yingwen Dong, Dong Wei, and Mark Rogge. "Pharmacokinetics of renally excreted drug dexpramipexole in subjects with impaired renal function." Journal of Clinical Pharmacology 54, no. 12 (July 3, 2014): 1383–90. http://dx.doi.org/10.1002/jcph.353.

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21

Ciceri, Samuele, Patrizia Ferraboschi, Paride Grisenti, Shahrzad Reza Elahi, Carlo Castellano, Matteo Mori, and Fiorella Meneghetti. "(S)-Pramipexole and Its Enantiomer, Dexpramipexole: A New Chemoenzymatic Synthesis and Crystallographic Investigation of Key Enantiomeric Intermediates." Catalysts 10, no. 8 (August 16, 2020): 941. http://dx.doi.org/10.3390/catal10080941.

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A new chemoenzymatic method has been developed for the synthesis of (S)- and (R)-N-(6-hydroxy-4,5,6,7-tetrahydrobenzo[d]thiazol-2-yl) acetamide, two key synthons for the preparation of (S)-pramipexole, an anti-Parkinson drug, and its enantiomer dexpramipexole, which is currently under investigation for the treatment of eosinophil-associated disorders. These two building blocks have been obtained in good yields and high enantiomeric excess (30% and >98% ee for the R-enantiomer, and 31% and >99% ee for the S- one) through a careful optimization of the reaction conditions, starting from the corresponding racemic mixture and using two consecutive irreversible transesterifications, catalyzed by Candida antarctica lipase type A. Single crystal X-ray analysis has been carried out to unambiguously define the stereochemistry of the two enantiomers, and to explore in depth their three-dimensional features.
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22

Coppi, Elisabetta, Daniela Buonvicino, Giuseppe Ranieri, Federica Cherchi, Martina Venturini, Anna Maria Pugliese, and Alberto Chiarugi. "Dexpramipexole Enhances K+ Currents and Inhibits Cell Excitability in the Rat Hippocampus In Vitro." Molecular Neurobiology 58, no. 6 (February 10, 2021): 2955–62. http://dx.doi.org/10.1007/s12035-021-02300-5.

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23

Prussin, Calman, Michael Bozik, James Mather, Donald Archibald, Steven Dworetzky, Randall Killingsworth, Sergei Ochkur, Elizabeth Jacobsen, Salman Siddiqui, and William Busse. "The Oral Eosinophil-lowering Drug Dexpramipexole Improves FEV1 Largely Thorough its Effect on FVC." Journal of Allergy and Clinical Immunology 149, no. 2 (February 2022): AB18. http://dx.doi.org/10.1016/j.jaci.2021.12.097.

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24

Buonvicino, Daniela, Giuseppe Ranieri, Sara Pratesi, Elisabetta Gerace, Mirko Muzzi, Daniele Guasti, Lorenzo Tofani, and Alberto Chiarugi. "Neuroprotection induced by dexpramipexole delays disease progression in a mouse model of progressive multiple sclerosis." British Journal of Pharmacology 177, no. 14 (April 18, 2020): 3342–56. http://dx.doi.org/10.1111/bph.15058.

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25

Urru, Matteo, Mirko Muzzi, Elisabetta Coppi, Giuseppe Ranieri, Daniela Buonvicino, Emidio Camaioni, Raffaele Coppini, et al. "Dexpramipexole blocks Nav1.8 sodium channels and provides analgesia in multiple nociceptive and neuropathic pain models." PAIN 161, no. 4 (April 2020): 831–41. http://dx.doi.org/10.1097/j.pain.0000000000001774.

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26

Laidlaw, Tanya M., Calman Prussin, Reynold A. Panettieri, Stella Lee, Berrylin J. Ferguson, Nithin D. Adappa, Andrew P. Lane, et al. "Dexpramipexole depletes blood and tissue eosinophils in nasal polyps with no change in polyp size." Laryngoscope 129, no. 2 (October 4, 2018): E61—E66. http://dx.doi.org/10.1002/lary.27564.

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27

Prussin, Calman, Tanya M. Laidlaw, Reynold A. Panettieri, Berrylin J. Ferguson, Nithin D. Adappa, Andrew P. Lane, Stella Lee, et al. "Dexpramipexole effectively lowers blood and tissue eosinophils in subjects with chronic rhinosinusitis with nasal polyps." Journal of Allergy and Clinical Immunology 139, no. 2 (February 2017): AB64. http://dx.doi.org/10.1016/j.jaci.2016.12.256.

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28

Wang, Bo, Xuyang Zhang, Jun Zhong, Shi Wang, Chao Zhang, Mingxi Li, Quan Hu, et al. "Dexpramipexole Attenuates White Matter Injury to Facilitate Locomotion and Motor Coordination Recovery via Reducing Ferroptosis after Intracerebral Hemorrhage." Oxidative Medicine and Cellular Longevity 2022 (August 4, 2022): 1–17. http://dx.doi.org/10.1155/2022/6160701.

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Deciphering the factors causing damage to white matter fiber bundles and exploring new strategies to alleviate white matter injury (WMI) is a promising treatment to improve neurological impairments after intracerebral hemorrhage (ICH). Ferroptosis usually occurs at perihematomal region and contributes to neuronal death due to reactive oxygen species (ROS) production. Dexpramipexole (DPX) easily crosses the blood brain barrier (BBB) and exerts antioxidative properties by reducing ROS production, while the role of DPX in ferroptosis after ICH remains elusive. Here, our results indicated that ferroptosis played a significant role in WMI resulting from iron and ROS accumulation around hematoma. Further evidence demonstrated that the administration of DPX decreased iron and ROS deposition to inhibit ferroptosis at perihematomal site. With the inhibition of ferroptosis, WMI was alleviated at perihematomal site, thereafter promoting locomotion and motor coordination recovery in mice after ICH. Subsequently, the results showcased that the expression of glutathione peroxidase 4 (GPX4) and ferroptosis suppressing protein 1 (FSP1) was upregulated with the administration of DPX. Collectively, the present study uncovers the underlying mechanism and elucidates the therapeutic effect of DPX on ICH, and even in other central nervous system (CNS) diseases with the presence of ferroptosis.
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29

Alavian, Kambiz N., Steven I. Dworetzky, Laura Bonanni, Ping Zhang, Silvio Sacchetti, Hongmei Li, Armando P. Signore, Peter J. S. Smith, Valentin K. Gribkoff, and Elizabeth A. Jonas. "The Mitochondrial Complex V–Associated Large-Conductance Inner Membrane Current Is Regulated by Cyclosporine and Dexpramipexole." Molecular Pharmacology 87, no. 1 (October 20, 2014): 1–8. http://dx.doi.org/10.1124/mol.114.095661.

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30

Cudkowicz, Merit E., Leonard H. van den Berg, Jeremy M. Shefner, Hiroshi Mitsumoto, Jesus S. Mora, Albert Ludolph, Orla Hardiman, et al. "Dexpramipexole versus placebo for patients with amyotrophic lateral sclerosis (EMPOWER): a randomised, double-blind, phase 3 trial." Lancet Neurology 12, no. 11 (November 2013): 1059–67. http://dx.doi.org/10.1016/s1474-4422(13)70221-7.

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31

Ferraboschi, Patrizia, Samuele Ciceri, Pierangela Ciuffreda, Maria De Mieri, Diego Romano, and Paride Grisenti. "Baker’s yeast catalyzed preparation of a new enantiomerically pure synthon of (S)-pramipexole and its enantiomer (dexpramipexole)." Tetrahedron: Asymmetry 25, no. 16-17 (September 2014): 1239–45. http://dx.doi.org/10.1016/j.tetasy.2014.07.011.

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32

Bozik, Michael E., Hiroshi Mitsumoto, Benjamin R. Brooks, Stacy A. Rudnicki, Dan H. Moore, Bing Zhang, Albert Ludolph, et al. "A post hoc analysis of subgroup outcomes and creatinine in the phase III clinical trial (EMPOWER) of dexpramipexole in ALS." Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration 15, no. 5-6 (August 15, 2014): 406–13. http://dx.doi.org/10.3109/21678421.2014.943672.

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33

Rudnicki, S., J. Berry, E. Ingersoll, D. Archibald, M. Cudkowicz, D. Kerr, and Y. Dong. "Dexpramipexole Effects on Functional Decline in ALS Patients in a Phase II Study: Subgroup Analysis of Demographic and Clinical Characteristics (P04.149)." Neurology 78, Meeting Abstracts 1 (April 22, 2012): P04.149. http://dx.doi.org/10.1212/wnl.78.1_meetingabstracts.p04.149.

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34

Gribkoff, V., D. Demady, E. Ingersoll, M. Bozik, and S. Frantz. "Human Dopamine Receptor Affinity and Potency In Vitro and Dose Tolerability in Beagle Dogs In Vivo of Dexpramipexole and Pramipexole (P04.150)." Neurology 78, Meeting Abstracts 1 (April 22, 2012): P04.150. http://dx.doi.org/10.1212/wnl.78.1_meetingabstracts.p04.150.

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35

Cudkowicz, M., L. Van den Berg, M. Bozik, E. Ingersoll, A. Coppell, W. Farwell, Y. Dong, and D. Kerr. "The EMPOWER Study: Design, Methodology and Baseline Features of the First Phase III Clinical Trial of Dexpramipexole for Patients with ALS (S25.004)." Neurology 78, Meeting Abstracts 1 (April 22, 2012): S25.004. http://dx.doi.org/10.1212/wnl.78.1_meetingabstracts.s25.004.

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36

Wei, Dong, Chichih Wu, Ping He, Doug Kerr, Scott Stecher, and Liyu Yang. "Chiral liquid chromatography–tandem mass spectrometry assay to determine that dexpramipexole is not converted to pramipexole in vivo after administered in humans." Journal of Chromatography B 971 (November 2014): 133–40. http://dx.doi.org/10.1016/j.jchromb.2014.09.029.

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37

Sacchetti, Silvio, Steven I. Dworetzky, Kambiz N. Alavian, Ping Zhang, Laura Bonanni, Armando Signore, Jamie Mangold, et al. "Decrease in a Leak Conductance Associated with Mitochondrial Complex V and Improved Bioenergetic Efficiency may Underlie Cytoprotection of at-Risk Neurons by Dexpramipexole." Biophysical Journal 100, no. 3 (February 2011): 459a. http://dx.doi.org/10.1016/j.bpj.2010.12.2701.

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38

Rudnicki, Stacy A., James D. Berry, Evan Ingersoll, Don Archibald, Merit E. Cudkowicz, Douglas A. Kerr, and Yingwen Dong. "Dexpramipexole effects on functional decline and survival in subjects with amyotrophic lateral sclerosis in a Phase II study: Subgroup analysis of demographic and clinical characteristics." Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration 14, no. 1 (September 17, 2012): 44–51. http://dx.doi.org/10.3109/17482968.2012.723723.

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39

Gordon, Paul, and P. Corcia. "Amyotrophic lateral sclerosis and the clinical potential of dexpramipexole." Therapeutics and Clinical Risk Management, August 2012, 359. http://dx.doi.org/10.2147/tcrm.s21981.

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40

"Dexpramipexole Dose-Ranging Biomarker Study in Subjects With Eosinophilic Asthma." Case Medical Research, August 6, 2019. http://dx.doi.org/10.31525/ct1-nct04046939.

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41

Zhang, Yibao, Qun Fu, Jiaping Ruan, Changxi Shi, Wuguang Lu, Jing Wu, and Zhiqiang Zhou. "Dexpramipexole ameliorates cognitive deficits in sepsis-associated encephalopathy through suppressing mitochondria-mediated pyroptosis and apoptosis." NeuroReport Publish Ahead of Print (January 23, 2023). http://dx.doi.org/10.1097/wnr.0000000000001882.

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42

"INSIDE INDUSTRY." Asia-Pacific Biotech News 18, no. 02 (February 2014): 47–58. http://dx.doi.org/10.1142/s0219030314000147.

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Abstract:
Fortis Escorts Heart Institute wins ‘Best Single Specialty Hospital - Cardiology‘ title. Probiodrug transfers its CDK9 inhibitor program to AstraZeneca. GE to expand in life sciences with acquisition of strategic assets from Thermo Fisher Scientific. MD Anderson teams up with Pfizer to advance cancer immunotherapy. Trovagene and US Oncology Research collaborate on a prospective study for urine-based KRAS testing in patients with metastatic pancreatic cancer. MedImmune and Immunocore enter immunotherapy agreement to develop novel cancer therapies. Nodality enters into a strategic collaboration with Johnson & Johnson Innovation in autoimmune diseases. Knopp Biosciences and NIH to collaborate in evaluating dexpramipexole in patients with hypereosinophilic syndrome. AMN Healthcare receives top workplace award. National Cancer Centre Singapore and Clearbridge BioMedics partner to bring circulating tumor cell technology closer to clinic. Latest updates on soaps, detergents, cosmetics, hair care industry at 4th Emerging HPC Surfactants Markets. CMT's 11th Phenol/ Acetone & Derivatives Markets in Shanghai, hones in on feedstock costs, excess capacities and more. A*STAR signs agreement with Nestlé to strengthen food & nutrition R&D in Singapore. Amorfix enters into agreement with a major global pharmaceutical company for Alzheimer's disease diagnostic. PHARM Connect Congress- One step before the future.
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"Panch SR, Bozik ME, Brown T, et al. Dexpramipexole as an oral steroid-sparing agent in hypereosinophilic syndromes. Blood. 2018;132(5):501-509." Blood 132, no. 13 (September 27, 2018): 1461. http://dx.doi.org/10.1182/blood-2018-08-870204.

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