기타 MOA들 (continued)

TargetTreatmenttype / MOATrial / sourcephasepatients / doseResult / DesignReference
Not Inosine trials but source data on uratePRECEPT Schwarzschild, 2008 #663) demonstrated non-futility of inosine treatment for slowing disability
Baseline SERUM URATE (mg/dL)UPDRS change (p/year)DATScan change (%/how long?)HR of reaching endpoint
<4.316.9-101 (reference)
4.3-<5.1
5.1-<5.8
5.8-<6.7
≥6.714.3-40.51
DATATOP
(Ascherio, 2009 #664) 2009
asch
Baseline SERUM URATEUPDRS change (p/year)DATScan change (%/how long?)HR of reaching endpoint
<3.9116.371 (reference)
3.91-4.60
4.61-5.20
5.21-6.20
≥6.216.120.64
Baseline CSF URATEUPDRS change (p/year)DATScan change (%/how long?)HR of reaching endpoint
<0.2417.471 (reference)
>0.57.220.65
Nilotinib원래 c-abl phosphorylates parkin → ↓parkin activityJAMA Neurology Study
Georgetown Univ
NCT02954978

Phase 2 NILO-PD Study
Parkinson Study Group, Tanya Simuni,
NCT03205488
P1OL
군당 25명(pcb, 150mg, 300ng)
(Pagan, 2020 #709) ↑CSF HVA, DOPAC (12 m), =
↑plasma DOPAC (12 M), =
CSF TOTAL AsYN (12M),
↓The ratio of CSF oligomeric/total α-syn,
(이외 Tau도 봄)

Shaltiel-Karyo et al. 2013 (reference column)
mannitol↓α-syn fibrils aggregation (
NZP437 (New Zealand Pharmaceuticals) next-generation bile acidMOA
  • xcvi) Aging등 → ↑ROS → Pathological cardiolipin remodeling (ie ↑ bad cardiolipin species) CL content in the brain decreases with aging,[24] and a recent study on rat brain shows it results from lipid peroxidation in mitochondria exposed to free radical stress. Another study shows that the CL biosynthesis pathway may be selectively impaired, causing 20% reduction and composition change of the CL content [25]→ membrane structure, mtDNA biogenesis, apoptosis, mitochondrial dynamics, It is also associated with a 15% reduction in linked complex I/III activity → mito membrane become leaky → ↓mito dysfunction
  • xcvii) NZP437 act on a target protein → ↑cardiolipin level in sPD fibroblasts, ↓mito ROS (in patient-derived DA iNeurons), ↓caspase 3, (in patient-derived DA iNeurons), restored ATP, MMP, [in vivo] MPTP mouse: restored cardiolipin level and MC1 activity (timing, sustainable effect?) (in SN and STRIATUM),
  • xcviii) (Phospholipid) cardiolipin is exclusively localized in the inner mitochondrial membrane,
Fibroblast (sPD
  • xcix) restored cardiolipin level
  • c) 기타 p10
patient derived DA iNeurones
  • ci) Normalized ROS
  • cii) Normalized caspase 3 activation
  • ciii) Normalized ATP, MMP 표
AD/PD 2021) compound A: INDUCEd DA neurons from fibroblasts Spd:
  • civ) ↑MMP
  • cv) =mitophagy
  • cvi) aSyn (→ 이 질문에 웬지 ATP5A8을 답변)
MPTP mice
  • cvii) restored cardiolipin
  • cviii) restored MC1 activity
  • cix) mt DNA?, mt proteins (TOM40) ? mc1 protiens?
  • cx) (design: Charlie at Oregon's chronic MPTP regimen, timing, sustainable effect?)
  • cxi) ATP,& MMP, 는 POSTMORTEM에서 못 봄.
  • cxii) DA neuronal loss?
  • cxiii) normalized DigiGait
NHP?
  • cxiv) 31P MRS: applicable to rodent, NHP? Protocol (any center)? Validated (spectrofluorometric enzymatic method vs imaging?)
CLINICAL PLAN
  • cxv) MC1 PET failed in Spd, why?
  • cxvi) Then Parkin-PD?
  • cxvii) WHY then 31 P MRPS?
Meeting 20210611
  • cxviii) Fibroblast: glycolytic pathway to generate ATP, so we replaced glucose with galactose in culture), VS iNEUrons: at first glycolytic pathway → (spontaneous change to during differentiation) oxidative phosphorylation
Confidential data packagePw: Jedi123. (case sensitive, . is part of the pw)
UDCANZP437
MOAlipid transporter of PA
CardiolipinDo not Restore cardiolipin levelRestore cardiolipin level
Caspase 33 level in iNeuronMild ↓NZP437 normalizes caspase 3 to that of age matched controls.
ATP assay10x more active in the ATP assay (?)
TargetTreatmenttype / MOAphasepatients / DesignResult / outcomesReference
RNAicxix) {Yang, 2021 #1319) 2nd: cause acute neurotoxicity in HNP
cxx)
exo-ASO4 (Exosome-mediated delivery of ASO4 )In vitro(Yang, 2021 #1319) primary neuronal culture, exo-ASO4 → HIGH cellular update, ↓aSyn mRNA & aggregation (both p- and unp- aSyn) induced by aSyn PFF
In vivo(Yang, 2021 #1319) A53T MICE, exo-ASO4 (ICV) → ↓aSyn mRNA & aggregation (both p- and unp- aSyn) aggregation,
↓DA ndgn
Cf) ASO is a single-stranded gapmer that can mediate sequence-specific cleavage of different types of RNA, including mRNA and non-coding RNA, targeted by the endogenous RNase H1.
ASO molecules can hardly pass through the cell membrane by itself and are likely to be degraded quickly by the proteases. Currently, multiple carriers, such as lipofectamine, liposomes, or lipid-based nanoparticles, are being used to deliver ASOs into the neurons
KM-819 (FAScinate)a potent inhibitor of FAF1, a key regulatory protein in cell death pathways, apoptosis, and necrosis, and leads to neuronal cell protection in pre-clinical studies. A higher level of FAF1 is found in PD patients and could contribute to the early cell death.
CVN424GPR6 inverse agonist, small molecule, - GPR6 is an orphan GPCR that has enriched expression in the striatopallidal, indirect pathway, MSN neurons of the striatum
- a target present in striatal neurons that express dopamine receptor D2. The company claims that CVN424 does not affect D1-dependent pathways, and that this selective targeting will help avoid LID associated with D1 activation. CVN424 is being developed as an add-on to L-DOpa
P2

P1

preclinical
2019, a Phase 2, randomized, place-controlled study began enrolling 66 people with Parkinson's who experience motor fluctuations on a stable dose of levodopa. To be eligible, patients must average more than 2 hours per day of "off time," i.e., periods when symptoms reappear between levodopa doses. Participants will be randomized to high or low dose drug or placebo, taken as an oral suspension once daily for one month. The primary outcomes are adverse events and safety measures; secondary outcomes include an unspecified efficacy measure, and pharmacokinetics. This trial takes place at 16 sites across the U.S., and is expected to end in 2020.
[Results]
Beyond meeting safety objectives, the drug achieved a significant and meaningful, dose-dependent reduction of "OFF time

2019, Cerevance completed a Phase 1 single- and multiple-dose safety study in healthy adults. Sixty-six volunteers received single CVN424 doses from 1 to 225 mg, or seven daily doses of 25, 75, and 150 mg or matching placebo. According to an April 2019 company press release, the drug caused no serious adverse events or changes in common safety measures including vital signs, cardiac function, and laboratory analyses.
(Brice, 2021 #1897)
MRx0005 and MRx0029 (4D pharma')orally delivered single strains of bacteria that are naturally found in the healthy human gut.P1multi-center, randomized, double-blind, placebo-controlled study

Rx0005 and MRx0029 are two unique single strain Live Biotheraputic candidates, which have been shown pre-clinically to have positive impacts on multiple key aspects of Parkinson's disease pathology, including gut barrier integrity, neuroinflammation, oxidative stress and neuroprotection. In animal models of Parkinsonian syndrome, 4D pharma demonstrated that MRx0005 and MRx0029, respectively protected against the loss of dopamine metabolites and dopamine-producing neurons in the brain.
nicotinamide riboside (NR), Haukeland UH and Bergenwas,nicotinamide adenine dinucleotide (NAD) replenishment therapyP1 NADPARK(Brakedal, 2022 #2012} DB, total 30 with early PD received 1,000 mg NR, NAD-precursor, or placebo for 30 days.--> led to a significant, but variable, increase in cerebral NAD levels—measured by 31phosphorous MRS—and related metabolites in the cerebrospinal fluid. NR recipients showing increased brain
NAD levels exhibited altered cerebral metabolism, measured by 18fluoro-deoxyglucose positron emission tomography, and this was associated with mild clinical improvement. NR augmented the NADmetabolome and induced transcriptional upregulation of processes related to mitochondrial, lysosomal, and proteasomal
function in blood cells and/or skeletal muscle. Furthermore, NR decreased the levels of inflammatory cytokines in serum and Csf
NE3107 (BY BIOVIE)Insulin resistanceP3

P2

Preclinical
•[plan이겠지]
NM202 Phase 3: Potential pivotal design to evaluate NE3107 promotoric activity in 200 patients starting L dopa or, depending on Phase 2 results, 200 patients that have received L dopa therapy for more than 3 years

Primary endpoint: MDS UPDRS parts 1 4

Phase 2 began Q1 2022 with possible topline data readout expected Q2 2022

NM201 Phase 2: Assess NE3107 promotoric activity while adhering to FDA requirement for a drug drug interaction study involving L dopa

40 patients with defined L dopa "off state", 1:1 active:placebo, 20 mg BID for 28 days

Safety assessments: Standard measures of patient health, L dopa PK and DDI

Efficacy assessments: MDS UPDRS* parts 1 4, Hauser ON/OFF Diary, Non Motor Symptom Scale

NE3107 Impact in Parkinson's Mice Models

Below table from (Biglan, 2017 #1563)

Uncertain Spans

  • “Aging등” (NZP437 MOA bullet xcvi) — second character reads as the Korean particle “등”; transcribed as printed.
  • “mannitol” row’s mechanism cell ends with an unclosed parenthesis “↓α-syn fibrils aggregation (” — preserved as printed.
  • “Fibroblast (sPD” — left-column label is missing the closing parenthesis in the source; preserved as printed.
  • “CVN424 … LID associated with D1 activation” — source prints “LiD” (mixed case); transcribed as “LID”.
  • “NE3107 (BY BIOVIE)” Preclinical row — sentence starting with “NE3107 Impact in Parkinson’s Mice Models” ends mid-thought; the continuation falls outside this page.