VTX3232 was well-tolerated with no dose-limiting toxicities identified. All TEAE were graded mild or moderate. VTX3232 exhibited a dose-dependent and dose-linear PK profile. Repeat doses of 3 mg QD maintained steady-state IL-1β IC50 coverage in both plasma and CSF over 24 hours. Repeat doses of 40 mg QD exceeded steady-state IL-1β IC90 coverage in both plasma and CSF over 24 hours. Robust, dose-dependent pharmacodynamic effects were observed in a whole blood ex vivo IL-1β stimulation assay. Additionally, reductions in inflammatory biomarkers were observed in plasma and CSF samples..

We expect to initiate a Phase 2a trial of VTX3232 in patients with early PD during the second half of 2024.

We also expect to initiate a Phase 2a trial of VTX3232 in subjects with obesity and certain additional risk factors for cardiovascular disease during the second half of 2024.
Ventus"brain penentrant" NLRP3 | Biomarkers of neuroinflammation upregulated in PD patients (slide)
  • Ventus is leveraging the Michael J Fox Foundation's biomarker initiative, Progressive Markers Initiative (PPMI), to inform biomarker selection
  • Ventus extracted data on prioritized disease-relevant biomarkers from the PPMI database for analysis
  • Data clearly supports that certain biomarkers of neuroinflammation and neurodegeneration are unequivocally upregulated in PD patients vs healthy volunteers

P1 ONGOING
Hv, sad, mad
VENT-02 was well-tolerated, with no dose-limiting toxicities or SAEs reported and only mild or moderate treatment-related adverse events observed. The moderate adverse eventsincluded headache and nausea and were only observed at a dose multiple times higher than the intendedtherapeutic doses.

VENT-02 demonstrated full target engagement through 100% inhibition of IL-1β in the blood in an ex vivo wholeblood challenge assay, signifi cant drug levels in the CSF for 24 hours, and reduction of inflammatorybiomarkers such as hsCRP. Based on the half-life and target coverage observed in the trial, VENT-02 hasdemonstrated the potential for once daily dosing.

Ventus expects to initiate a Phase 1b trial of VENT-02 in patients with PD in the second half of 2024 and a Phase 2 trial in patients with treatment-refractory epilepsy in 2025.
RocheRO7486967, RG-6418/ZD334/RG6418/Selnoflast/RO7486967
Kp,uu: 0.06~0.1

(Roche pipeline widget thumbnail)
ISRCTN85338453 https://doi.org/10.1186/ISRCTN85338453
Phase 1b adaptive multicentre double-blind randomized placebo-controlled parallel design study
Recruitment start date:15/07/2022
Recruitment end date:15/07/2023
, idiopathic PD 50 to 85 years (early PD), TSPO-PET will be used.
Treatment Period of approximately 28 days
Group 1 will receive RO7486967 given as two pills in the morning and two pills in the evening every day for about 4 weeks.
Group 2 will receive a placebo given as two pills in the morning and two pills in the evening every day for about 4 week
There is nothing listed on clinicaltrials.gov for selnoflast (RO7486967) but on the Roche web page they list the PD study as "Not yet recruiting". The study number is BP43176 and its states that it will run in 3 countries (Netherlands, UK and USA). See https://forpatients.roche.com/en/trials/neurodegenerative-disorder/pd/a-phase-1b-adaptive--multi-center--randomized--double-blind--pl.html.

On the NHS web page (https://www.hra.nhs.uk/planning-and-improving-research/application-summaries/research-summaries/bp43176-ro7486967-in-participants-with-parkinsons-disease/) it lists the date of the Rec opinion as March 9, 2022 and that it will run for 2 years.

On the ISRCTN registry web page (https://www.isrctn.com/ISRCTN85338453) it is listed as recruiting. The start date is listed as 4/11/2021 and the end date is listed as 10/30/2023.
[ex-vivo stimulation with LPS] and rapid inhibition of IL-1β release following the first oral administration
Blood]
C-Reactive Protein (CRP) levels decreased slightly upon treatment, with a mean (± SD) change from baseline at Day 7 of -1.8 (±3.65) mg/L compared to +0.51 (±1.43) mg/L in the placebo arm. However, this decrease was driven by one outlier and was not considered clinically significant. Plasma levels of IL-1β were below the limit of quantification. There were no significant changes in plasma IL-18 levels upon treatment. [Colon] However, there were no significant reductions in neutrophil numbers in either study arm (results not shown). Caspase-1 (pro- and active forms) did not show marked changes after 7 days' treatment with selnoflast (data not shown).
Nodthera
NT-0796, Phase 1 ongoing (BBB only potential) Prodrug: NT 0796 (ester) forms a bioactive acid (NDT 19795) intracellularly, IC50 NDT19795 (PBMC) 52 nM,

Structure disclosed last week at a chemistry conference in UK (communication with Steve Woodhead)
P1b/2a TrialTroveID-474806
HV → PD, results in PD pending
The initial stage of the study, in HEV, is already underway, investigating a modified formulation of the drug candidate designed for use in the upcoming patient arm of the study.
The study is exploring the candidate's effect on inflammatory and disease-specific biomarkers in the blood and CSF using an innovative clinical biomarker panel, designed using the preclinical profile of NT-0796 on cytokines, chemokines, markers of microgliosis and astrogliosis relevant to NLRP3 inhibition.
Subjects in the study were cannulated and CSF-sampled on Day 1 (pre-dose) and Day 7 following daily NT-0796 dosing.

In four elderly HV (out of 7), ↓ CSF NFL in 7 days: ↓ by approximately 25% over 7 days in the most inflamed subjects by 13% on average
[PD study results]
NodThera's study demonstrated mean reductions of key pro-inflammatory biomarkers in CSF (e.g. IL-1β, IL-6, CCL2, CXCL1 and CXCL8 (=IL-8)) over 28 days compared to baseline to levels approximating those of healthy elderly controls. In addition, reductions in neurodegenerative markers were also observed following oral dosing of NT-0796, including NfL and soluble TREM (sTREM2).

[note]
TREM2 (triggering receptor expressed on myeloid cells 2) is a transmembrane innate immune receptor of the immunoglobulin family, which is found on microglia in CNS. This receptor also undergoes proteolytic cleavage to generate a soluble form (sTREM2), the abundance of which is increased in CSF of AD patients. Furthermore, the R47H and R62H mutations in TREM2 are associated with a statistically significant increase in the risk for developing AD. Zhong et al. found that sTREM2 promoted the survival of mouse microglia in vitro by blocking apoptosis when the cells were deprived of GM-GSF, a cytokine that promotes viability. sTREM2 also promoted the expression of genes encoding proinflammatory cytokines in cultured microglia. The ability of sTREM2 to promote microglial survival depended on signaling by the kinase Akt, whereas proinflammatory cytokine production depended on activation of the transcription factor nuclear factor κB. Last, when administered to the hippocampi of either wild-type or TREM2-deficient mice, sTREM2 stimulated inflammatory cytokine production and induced morphological changes in the microglia consistent with activation.
Healthy elderly control levels set to 100%%reduction from BL to 100%
IL-1bIL-6IL-8CCL2CXCL1NFLsTREM2
Relative level to HE (%)%reduction from BLRelative level to HE (%)%reduction from BLRelative level to HE (%)%reduction from BLRelative level to HE (%)%reduction from BLRelative level to HE (%)%reduction from BL%reduction from BL (median)%reduction from BL
Day 11807611511382
Day 780-56%60-21%95-17%90-20%70-15%70.1
Day 2895-47%35-54%101-12%85-25%75-9%10.5
Sem not SD, No statistical testing (don't know whether significant), don't know detection ratio, NFL & Stream not significant. Overall, only IL-6 reduction seems potentially meaningful.
obesitythe first patients have been dosed in a Phase Ib/IIa clinical trial evaluating the potential of its lead candidate, NT-0796, to assess cardiometabolic biomarkers in obese patients with risk factors for atherosclerotic CV disease. This follows a "no-objection to proceed" letter in response to the Company's IND application.
The randomised, double-blind, placebo-controlled Phase Ib/IIa trial will evaluate the pharmacokinetic and pharmacodynamic (PK/PD) profile of NT-0796 in inflamed obese patients over 28 days. Up to 60 patients will be enrolled and randomised into two cohorts receiving either NT-0796 or placebo. The study's primary endpoint is the change in baseline to Day 28 of high-sensitivity CRP levels, a key peripheral inflammatory marker and known predictor risk of developing atherosclerotic CV disease. Secondary endpoints include multiple inflammatory and CV-risk specific biomarkers
FIH, P1 sad complete
ACTRN12621001082897
Favorable potency: ED50 of 2mg/kg, EC50 of 74 nM,
PoC study in RRMS to SPMS and ALS delineated
Confirmed an excellent PK/PD profile, brain penetration and anti-inflammatory effects in HV.
↓ stimulated IL-1β/IL-18 and inflammatory biomarkers (hsCRP and fibrinogen total blood, ex-vivo, ↓ IL-...) confirms dose dependent pharmacodynamics

MAD: ↓ Plasma CRP (not balanced between placebo and Tx group)

- CUPRIOZONE MODEL: ↓ plasma NFL, ↓ plasma GFAP
NT-0249, Peripherally restrictedMAD completed (HV)↓ key inflammatory biomarkers, C-reactive protein (CRP) and fibrinogen,
Levels of NT-0249 measured in the CSF additionally demonstrated high levels of brain penetration
FIH, https://anzctr.org.au/ACTRN12622000195752.aspx
• NT-0527 DC, declare in 1Q22Fully brain penetrant
las Inflazome is also developing an NLRP3-targeted PET tracer, with funding from the MJF (press release). Patent has PD data.
950 ID-3 CP-73) Directly bonds to the NACHT domain and changes NLRP3 confirmation

MCC950 reversibly binds to NLRP3 protein
blocks NLRP3 activation at nanomolar concentration [64].
MCC950 directly bonds to the WALKER B region on the NACHT domain of NLRP3. The binding of MCC950 changes confirmation of NLRP3 to a "closed" state as detected by bioluminescence resonance energy transfer (BRET) method [21].

MCC950 directly interacts with the Walker B motif within the NLRP3 NACHT domain, thereby blocking ATP hydrolysis and inhibiting NLRP3 activation and inflammasome formation.
MCC950 → ↓ NLRP3 oligomerization,
The number of NLRP3 oligomer

Closed (resting, ↑ BRET signal) vs open (activated): BRET assay (Tapia-Abellán, 2019 #1770)
Monomer vs oligomer
MCC950: resting NLRP3에도 좀 붙는 듯 ((Tapia-Abellán, 2019 #1770)
(Coll, 2019 #1771)
MCC950 binds non-covalently to NLRP3, proximal to the Walker B motif and blocks NLRP3 ATPase activity

MCC950 specifically binds to both active and inactive NLRP3,

Uncertain Spans

locationtranscriptionuncertainty
Ventus row, embedded slide chartfour-panel scatter plot icons under “NLRP3 | Biomarkers of neuroinflammation upregulated in PD patients”Slide is small inside the cell; only the title and the three bullet captions are legible.
Roche row, pipeline widgetcolour-tagged stage labelsStage chips read like “P1b study planned / completed / ongoing” but specific compound names beside chips are below legible threshold.
Nodthera Day 7 / Day 28 grid%reduction from BL columnsSeveral percentage values (e.g. Day 28 NFL = 10.5) are at the edge of the cell; preserved as best-effort.
Nodthera narrative “ED50 of 2mg/kg, EC50 of 74 nM”numeric valuesBoth values appear faint near the edge of the cell.
Halia row leftmost cell labelreads as “las”The owner-name token at the start of the row is partly cut off; recorded as “las” (likely tail of “Halia”).