Det er nok noen som er redd dataene skal slå negativt ut, eller selge på news.
Edit:
Men skal en tolke smilefjesene i dag, tror jeg ikke det 
Det er vel bare emi gutta som skal ut ! Får håpe de står for mesteparten av salg på mandagens liste 
Vi tror at aksjekursen kan være på et vendepunkt, da mange kliniske prøveutlesninger nærmer seg
Dagens fra DnB,
Targovax reported an operating loss of NOK40m for Q1, bang in line with our estimate. On the conference call, management highlighted prospects of near-term readouts from several clinical studies. It also said data from the mesothelioma trial will be presented around New Year 2020, sooner than previously communicated. We keep our BUY recommendation but have cut our target price to NOK10.5 (13) following the recent private placement.
Q1 operating loss of NOK40m . Including the recently received proceeds from the private placement, Targovax had cash of NOK172m at end-Q1, enough to run operations towards the end of 2020 on our calculations.
We expect a lot of near term news flow from clinical activities . Management said on the Q1 conference call that it expects to communicate the data readout from the Melanoma trial with ONCOS-1012 before the end of June this year. The data will focus on ORR and immune response in patients from the first cohort of the study. The company is aiming to present 3-year survival data from the phase I/II trial with TG01 in patients with resected pancreatic cancer in about two weeks. What caught our attention during the conference call was that randomised data from the ONCOS-102 phase IB/II trial in unresectable mesothelioma will be presented around New Year 2020, according to management, sooner than had previously has been communicated and a result of faster patient recruitment than expected. On 8 May Targovax reported that enrolment in the study had been completed and it is now awaiting 6-month survival data from all patients before the readout can be communicated.
Out-licensing to Zelluna Immunotherapy . During Q1, Targovax granted Zelluna Immunotherapy an FRO licence to the intellectual property relating to mutant RAS T-cell receptor technology. During the conference call, management clarified that it does not expect any milestone payments from this deal near-term, but that it would have an option to participate in Zelluna Immunotherapy’s potential future success with its technology.
We reiterate our BUY recommendation but have cut our target price to NOK10.5 as a result of the average number of shares rising from c52.6m to c63.1m following the recent private placement.
10/05-2019 07:00:06: (TRVX) Targovax ASA: Commencement of subscription period in the subsequent offering
Ikke lett å vite hva man skal gjøre når kursen er 6,30, reparasjonsaksjer til 7kr og mellom der en avlesning som kan trigge opp eller ned. Snittet ned i går, bare 9,90 i kostpris 
Sånn, da fikk jeg tid til å¨skrive det som var tiltenkt. Årsaken til at ledelsen ønsket å utvide tegningsperioden var vell nettopp for at vi skulle få TG01 meldingen først, i håp om at det skulle booste kursen over de 7kr som reperasjonsaksjene er satt til. Aksjonærvennlig tanke. Jeg håper jo de får inn de pengene, men er selv usikker på hva jeg skal gjøre med aksjene per nå, ettersom vi er under tegningskursen. Forhåpentligvis flyr vi over 7kr, slik at det blir et godt kjøp, og ledelsen får inn de sårt trengte pengene
Jeg har nå tegnet meg, det er jo mulig å annullere om kursen ikke når over 7,-
Det bruker ikke å være mulig å trekke tilbake tegningen etter at det er sendt inn.
Se tegningsskjemaet like over signaturfeltet:
I/we hereby irrevocably (i) apply for the number of Offer Shares specified above subject to the terms and conditions set out in this Subscription Form and in the Prospectus,
Irrevocably = ugjenkallelig
Edit: og det står det samme litt lenger oppe på skjemaet
Subscriptions are irrevocable and binding upon receipt and cannot
be withdrawn, cancelled or modified by the subscriber after having been received by DNB Markets, or in the case of subscriptions through the VPS online subscription system, upon
registration of the subscription.
Avventer först Q1 for Pho og nyheter fra Trvx för jeg bestemmer meg om aa nulle ut, bruke rettene eller overtegne. Ett eller annet sted maa ev penger tas.
Igår sa de at dataene kommer om 2 uker (ca?). Det vil si 23 mai, tilfeldigvis samme dag som Magnus skal på AX Exposure, live webcast… mulighet for å tenge seg aksjer på nok 7 går ut 24 Mai… tipper det blir en ganske heftig volum den 23 da… får håpe man blir kvitt de kortsiktige i samme slengen…
ok, takk busk1. Så bare i VPS at det var en knapp det sto “annuller” på.
Har du mottatt skjema i posten ?
For min egen del er jeg villig til å ta ett (midlertidig) papirtap for at selskapet kan få frisk kapital rett i kassa. Dette skjer jo som kjent ikke om man kjøper i markedet.
Vil først se an en evt. positiv/negativ mld.
Er egentlig fullastet, men…
Hva vil være positivt/negativt?
9/13 fra 2 års ilivet…
Realistisk så tenker jeg vi har 5-6 av 13 ilivet for cohort2. Håpet selvsagt på 7+/13 for lengere mOS…
Mit perspektiv for at akkumulere på 6-tallet er, at det er ganske få uger siden, aktien blev handlet i rekordhøj volumen på 11-tallet (endda med forestående emission …). Her ser man nu dagligt aktører i markedet sælge store poster på 6-tallet … uden forestående emission.
Jeg satser på gode data fra TG-01 3-års udlæsning. Det er svært at se, hvordan det videre forløb for TG-01 ser ud, men aftalen med Parker og CRI har vist, at der rent klinisk er stor interesse for de resultater, selskabet har præsteret. Det er min vurdering, at denne interesse på sigt kan og bør blive omsat til interesse fra BP - og blive en gevinst for patienterne.
En tydelig 3-års forsættelse af “halen” jfr. 2-års udlæsningen vil nok tiltrække sig stor opmærksomhed og med rimelighed bruges som forhandlingsgrundlag overfor en partner, der enten ønsker at tage TG-01 ind i egen portefølje eller indgå i et samarbejde om et større klinisk studie (med mDFS som endepunkt jfr. Sougs udtalelser på Q4 præsentationen).
I tillæg til ovenstående har ledelsen jo indikeret en relativ stærk nyhedsstrøm for resten af 2019, så jeg ser personligt ikke nogen udfordringer i at akkumulere med 10 - 15% rabat på emissionsniveauet.
Q1 presentation 9 May 19
Ladies and gentlemen, welcome to this quarterly presentation of Targovax. Welcome to the people in the room. Welcome to people on the web. My name is Øystein Soug, and with me today, I have our CFO, Torbjørn Furuseth.
I suspect that most of the people listening into this, they are familiar with our technology. But for the benefit of those who are not too familiar, I will give you a short introduction to who we are and what we are doing.
And what you see on this slide is an overview of the cancer therapy landscape, the way we picture it today. It’s a map of what’s happening in cancer treatment. And of course, still, surgery, radiotherapy and chemotherapy plays a very central role in treating cancer patients. But immunotherapies are getting an increased usage all around the world. And particularly checkpoint inhibitors, immune modulators, they are proven to be very important in the cancer treatment. Many patients today rely on checkpoint inhibitors in their treatment. And not only is it a good thing for the patients, it’s also commercially very viable, what’s happening with the checkpoint inhibitors. In 2018, 2 of the 3 most best-selling cancer drugs were checkpoint inhibitors.
But there’s a growing body of evidence suggesting that in order for the checkpoint inhibitors to have effect in more patients, they need to be combined with immune activators. And the reason behind that is that checkpoint inhibitors, they don’t kill cancers. They create an environment that enables T-cells to kill cancers. But if the patient doesn’t have enough T-cells or the right T-cells in a tumor marker environment, the checkpoint inhibitors are not going to work. So it’s probably a good combination to combine immune activators and checkpoint inhibitors.
And we have 2 immune activators in our portfolio. The lead product candidate is an oncolytic virus called ONCOS-102. Now that is a cold virus that we have genetically modified in order to kill cancers. So what we do is to inject this virus into the tumor of the patient. The tumor lysis breaks up, and everything inside the tumor is being released into the patient’s body. And what’s important in that tumor in the cancer cell is something called antigens. And the antigens, they are like the fingerprint or the barcode of the cancer, telling the immune system what type of T-cells need to be produced in order to kill that cancer. And we have 4 ongoing combination trials with ONCOS-102.
We also have a neoantigen vaccine. So that is not a prophylactic vaccine. It’s a therapeutic vaccine that you can use after patient has cancer. But whereas the virus lysis, the cancer cells releases antigens that way, with the vaccine, we have created antigens in the lab that mimic the antigens that certain cancers will produce. And in this case, we have picked out mutated RAS as our target, which means that this vaccine could be applicable in some 20% to 30% of all cancer cases. We think it’s a very good target because RAS is also a cause of cancer. It’s a driver mutation. And then this – with this platform, we have one trial recently completed, and there’s one small trial ongoing.
Both these platforms, both these drugs, they are off the shelves. So there’s no need for an expensive or logistically-heavy individualization in order to make this work. They are patient-specific nonetheless but can be taken off the shelf.
Now to the quarter. These are the highlights of the quarter here on the screen right now. And the first bullet here relates to the melanoma trial that we’re running with ONCOS-102. Now that is a trial we are in – that we’re doing in checkpoint inhibitor refractory patients. That means patients who have stopped responding to checkpoint inhibitors or never responded to a checkpoint inhibitor probably because they don’t have enough of the right T-cells in their tumor marker environments. And the idea here is that we give them ONCOS-102 to produce more T-cells and then put them back on a checkpoint inhibitor and see what happens.
This trial has 2 cohorts, 1 cohort where they get 3 rounds or 3 injections of ONCOS-102. And there’s a second cohort, which we are – which we just started this quarter, where we increased the number of ONCOS injections from 3 to up to 12. So we have high hopes for this trial. Just to remind you, in the first cohort with few injections, we had 1 complete response. And there will be data on this trial later this year and also in 2020.
The second bullet has to do with the mesothelioma trial. Just a few days ago, we sent out a press release saying that, that trial is now fully recruited, 31 patients. That means that the timelines are now a bit more fixed. And when to expect the data, we are just sitting now and waiting for the data of that trial. And we are now expecting that to be a few months from now.
The third bullet relates to our new viruses. And we haven’t talked too much about the new viruses previously. The targets are undisclosed. They still are. But now we feel that we have gone so far in the development of these new viruses that it’s possible to say a few more words about them, and I’ll do that later in the presentation.
On TG. We signed a collaboration agreement with the Parker Institute and CRI. We sent a press release on that a month ago. What – the intention of that collaboration is to start a trial in advanced pancreatic cancer. And not in resected where we have done trials before, but the advanced pancreatic cancer. That’s also an exciting development for us.
On the corporate side, patents. We had 2 patent news. One relates to the combination patent of TG with chemotherapies in Europe, which was granted. And in the U.S., we got a Notice of Allowance of a composition of matter patent for TG02 and TG03, which is good news.
Also, we work with Zelluna, which is another Oslo-based biotech company that develops RAS TCRs during the quarter and agreed with them to give them the license they need in order to develop their technology within our – or the field of mutant RAS. So that is a deal with a possibility for us to participate in Zelluna’s success going forward. So there’s no payments now in the short term. But if Zelluna is successful, we will be able to take part of that in the future.
And last but not least, we raised an important NOK 74 million in a private placement in March.
So what you see here is the total program of what we’re doing. The 2 most important trials are on top, the mesothelioma trial and the melanoma trial. And as I mentioned, there are 2 cohorts in the melanoma trial. The first cohort with 3 injections will have a readout before the summer. So it’s 9 patients that we will give you a fairly good data set, both ORR and immune activation data for these patients. We have given you some data on the first 6 patients. Now you will get most of the data for the first 9 patients.
But mesothelioma on top. Probably the indication where we – or this indication where we think is the shortest path to market for us. So it’s an important trial in that respect. And the recruitment of patients in this trial was better than expected. So our previous guiding was the first half of 2020. And now we’re changing that guiding to around new year. So that means that could be before new year. Could be after. But plus/minus, new year is when we expect that data. As I said, the patients are already in. We’re just waiting for them to reach 6-month survival and then to process the data when we get it.
Three new viruses. We will talk more about that. But in order to explain to you the modalities of the new viruses, just to remind you what ONCOS-102 is. And as you can see here up in the right-hand corner of this picture, there is a portrait of a virus. That’s what they actually look like in the bile. It’s a photography, if you like, of the viruses. And on the bottom, we have a schematic overview of what the viruses look like. And so this is a virus, which exists in the bile. It causes flu-like symptoms when the patient get it. And what we have done is to do 3 adaptations that are needed for cancer treatment. So one here under the number one, selective application, is an adaptation, a genetic modification we have done in order to ensure that the virus only replicates in cancer cells, not in healthy, normal tissue. And number three here, enhanced infection of cancer cells, is just to ensure – it’s a modification we have done in order to ensure that, as it says, enhance – infects cancer cells better. But the most important adaptation is the transgene. So the primary function of an oncolytic virus is to lyse the cell. It’s to break up the cells and release the antigens. But when you have a virus-like an immuno virus where you can put in a transgene, you can also add on additional modalities to what the virus is doing. And if you put in a drug as a transgene, it will also be replicated when the virus replicate. And the effect of that is that you can produce or you can create an in-patient factory of a drug if you use that drug as a transgene. So that creates some opportunities.
And in ONCOS-102, we chose GM-CSF because GM-CSF has the function of attracting APCs, or antigen-presenting cells and dendritic cells, to the tumor sites whose function it is to take the antigens to the lymph nodes where the T-cells are being produced. So it enhances the activation of the immune system by using GM-CSF. It’s an important modality. It’s a good modality. But there are other ways, other modalities, that you could also investigate. And that’s what we have been doing now with our 3 new viruses.
The first one is ONCOS-211. It counteracts immune-suppressive tumor microenvironment. Now what that means is that cancers, cancer tumors, they have ways to protect themselves against the immune system. And one way of doing that, which is well known, is the checkpoint PD-L1, which tells T-cells not to attack. And of course, the checkpoint inhibitors, the PD-1 checkpoint inhibitors, they are created in order to counteract that measure that the cancer uses to protect themselves. That’s one way of doing it but the cancer has other ways of protecting itself as well. And these 2 transgenes that we have in ONCOS-211, they try to counteract that protection that the cancer mounts against the immune system.
The second virus, ONCOS-212, inhibits the tumor growth and vascularization. Now tumors, like any other parts of a patient’s body, they need oxygen. And these cells, they also need all the nourishment. And that comes partially through the blood vessels and partially through other means into the tumor cells. And the 2 transgenes that we have in this virus, they try to stop that flow of oxygen to nourishment. So in a way, we’re trying to starve the cancer cells. It’s a well-known function and in use also in other drugs in cancer treatment.
And last but not least, we have ONCOS-214, which probably is the more innovative one, and my personal favorite. In that it enhances cell-killing properties. Now as I mentioned, the primary function of an oncolytic virus is to lyse the cells, to break up the cells. But you can put it in other transgenes, we can put in drugs as transgenes that will kill cancer cells in other ways as well. So that will enhance the cell killing and release more antigens quicker.
So these are the modalities. This is what the new viruses do. We are past in vitro testing on all of them, and we are into in vivo in all of them as well. And we’ve passed also the first stage of in vivo testing on ONCOS-212. So there they are some data. And as I mentioned previously, later in the year, we will release data on all these viruses.
Very exciting. And with that, I give the word to Torbjørn to take you through the developments on the finances and the mutant RAS battle.