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That delay is the problem jiving, we know they need to go through all the phase trials which was going to see the product get to market in 2029 at the earliest. Now we have effectively been delayed by a year, so phase 1 ready would be end of 2023 following non-glp and glp toxicology studies.

Meanwhile AZ are pushing forward with Saracitinib for IPF, going into phase 1 trials and already have orphan drug designation.

The below are the two poster session papers being presented at the up coming ERS on 6th Sept, 8.30am to 9.30am.

In vitro and ex-vivo evaluation of anti-inflammatory and anti-fibrotic effects of NXP002 in rat and human cells and lung tissue

Simon Cruwys, Mark Saunders, Alastair Riddell, Bob Humphries

Introduction

These studies investigated anti-inflammatory (AI) and anti-fibrotic (AF) effects of NXP002, a new salt form of tranilast and potential novel inhaled treatment for Idiopathic Pulmonary Fibrosis (IPF), in rodent and human cells and lung tissue.

Methods

Freshly isolated rat splenocytes or human peripheral blood mononuclear cells (PBMCs) were incubated with NXP002 (1 to 3000 µM) prior to stimulation with LPS (100 ng/mL). Inflammatory and fibrotic mediators were measured by Luminex multiplex 4 and 24 hours after stimulation.

Precision-cut lung slices (PCLS) were prepared from Sprague Dawley rats. Inflammatory and fibrotic responses were induced with LPS (1µg/ml; 24hrs) or TGF-ß1 + PDGF-ßß (3µg/mL and 50ng/mL; 72hrs). The effects of concomitant administration of NXP002 (75, 150 or 300µM) on inflammatory cytokines, measured by ELISA, and tissue fibrosis marker gene expression by qPCR was assessed.

Similar assessments were made in PCLS prepared post transplant from 6 end stage IPF patients.

Results

NXP002 concentration-dependently inhibited LPS-induced cytokine production (IL-6, IL-10, MCP-1) by rat splenocytes and human PBMCs.

In rat PCLS, NXP002 concentration-dependently attenuated LPS induced MCP-1 and dampened IL-6 secretion, and attenuated TGF-ß1 + PDGF-ßß induced upregulation in collagen 1 and aSMA gene expression.

NXP002 demonstrated an AF effect in human IPF tissue, with reduced production of MCP-1, Col1a1 and fibronectin.

Conclusion

NXP002 consistently demonstrated AI and AF effects in rat and human cells and lung tissue. Reductions in key biomarkers of fibrosis in IPF tissue support further evaluation of NXP002 as an inhaled therapy in IPF.

Inhaled NXP002 attenuates LPS-induced inflammatory and fibrotic mediator production in the rat lung

Bob Humphries, Mark Saunders, Simon Cruwys, Bob Humphries

Introduction

Oral tranilast has been shown to attenuate fibrosis clinically but has limited use due to low bioavailability and systemic side effects. NXP002, a new salt form of tranilast, is a potential novel inhaled treatment for Idiopathic Pulmonary Fibrosis (IPF). These studies assess the distribution, tolerability and efficacy of NXP002 in the rat.

Methods

NXP002 was administered by inhalation (Cirrus 2) to Sprague Dawley rats at target lung deposited doses of 0.1, 0.3 and 1 mg/rat. NXP002 (10 mg/kg) was also dosed orally. Inhaled Fluticasone propionate (FP, target 0.3 mg/rat) acted as a positive control. Animals were then challenged with aerosolized LPS (1 mg/mL).

Animals were culled 4 h post LPS challenge and blood samples taken. Bronchoalveolar Lavage (BAL) was obtained, centrifuged and the supernatant collected for bioanalysis, cell counting and mediator determination. NXP002 levels in plasma and lung homogenate were determined.

Results

Inhaled NXP002 was well tolerated, with no inflammatory response observed. Dose-dependent increases of NXP002 in lung tissue and BAL were observed, equivalent to or higher than following oral administration despite lower plasma levels.

Inhaled NXP002 resulted in a dose-dependent decrease in LPS-induced BAL cell count, which was less than that seen following oral delivery. Despite this, inhaled delivery resulted in a greater reduction in LPS-induced BAL mediators, including MCP-1 and TGFß.

Conclusions

This study demonstrates that inhaled NXP002 is well tolerated. Inhaled delivery has a superior effect on fibrosis related mediators whilst having a reduced systemic exposure than oral dosing.

Sorry Mars, the company has always had a resolution to allow share buybacks at every agm since they listed. It’s standard. Always has been there. Nothing to get excited about.

Standard resolution. Same as the one allowing them to issue up to 3m quids worth of shares.

Exactly the same trade that was made back on 4th August and then cancelled.

Thats what the AGM is for no?

Really, is that why yesterday there were 12m+ shares traded before 1pm and less than 1.3m traded after?

Tip… yanks buy at all times of the day…. If they’re buying. They don’t wait for any particular time.

Hargreave, you do know that NXP002 is not due on the market till at least 2031? Hence the company have said long Covid is not their focus.

Interesting to see some relative strength in buying today, although still below where it was a week or so ago, so nothing to be too excited about.

May hear a bit more before the agm to give some good vibes for the one person who shows up.

Off down to the south of France tomorrow anyway so won’t be meet attending.

lol! They're now twitting GSK, Pfizer and AZ to ask them if they are looking at NFX.

Because obviously the social media person in marketing makes those kind of decisions.

Someone on twits seems to be having some sort of breakdown and jabbering on to randoms about Dan being back.

Takes all sorts I guess.

If peoples timeframe is 40 mins, then a stock with this spread is the most ridiculous stock to try and trade, you'll never win.

beat me to it filter.

At least the 1.2m sell was someone who bought on 15 July for 0.388p

Doesn't help when somebody only olds for 40 minutes!

845,102 bought at 12.13 for £4969 then they sold just now at 12.53 for a 600 quid loss.

Given the spread its about 9% up.

Somewhat bonkers they aren't raising the bid given the scale of buys. Likely a big sell being absorbed by them.

Zero chat elsewhere on this as well.

All part of the conundrum

No dirty games, just traders who bought the rise jumping out.