Assembling my biofolio...
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ARQL. www.abstractsonline.com/pp8/?utm_source=sendgrid.com&utm_medium=email&utm_campaign=mention#!/4562/presentation/11137
RTTR—The upward move at the end of the AH session could be a head fake by a large investor who wants to dump shares at the open tomorrow.
The PR is a joke and the stock deserves to be down.
ALXN acquires WTX.ST for SEK 232/sh—a 70% premium to yesterday’s close
MNLO phase-2 for MTI-103 in pruritis/AD fails
CALA -
NLNK (who also has an IDO1 drug) -37% on INCY news.
AIMT - 3/27/18 Needham CC notes
1. Regarding potential pricing for AR101 for peanut allergy, during the 6-8 month period where intense up-dosing is required, AIMT expects pricing of $5,000 - $10,000 per patient.
2. For subsequent maintenance phase, AIMT expects monthly pricing of $300-$500 per patient.
3. For the initial year, AIMT estimates total pricing of $10,000 per patient.
4. For subsequent years, AIMT estimates total pricing of $4,500 per patient per year.
5. AIMT estimates 100,000 - 150,000 new patients per year as addressable by AR101.
Inasmuch as the phase-2 flu data looked good on both safety and efficacy, the lack of external interest in the program is an enigma.
You meant, norovirus, which VXRT refers to as the lead program.
VXRT -
Yes, indeed, provided the efficacy is as good (or better).
ARNA -
Oasis was a randomized trial and while there were some minor age differences between arms as it happened, I don’t think that was significant.
Re: ARNA P2 etrasimod data -
ARNA CEO Amit Munshi will present tomorrow 3pm at the Needham Healthcare conference.
VRNA +41% on phase-2b data in COPD maintenance
Re: ARGX/(MNTA)
ARGX-113 is the main competitor to MNTA’s M281, according to MNTA, but M281 more strongly engages the receptor than ARGX-113 (according to MNTA).
Re: CCXI/IFRX/ACHN -
It is curious that CCXI management did not mention these types of data in their discussion of C5a/C5L2 receptor selectivity and function in kidney diseases, as they are also pursuing C3G disorders. My complement bet here continues to be ACHN.
Re: ADXS -
One day after our thread in Jul 2017, ADXS’ CEO was canned. Since then, no one at ADXS (to my knowledge) has asserted that the NEO program will use a “brute force” method and thereby avoid an antigen-selection algorithm. So, it appears to me that the brute-force idea was bogus from the get-go and was a gimmick to hook unsophisticated investors.
I’m revisiting this thread now because the phase-1 ADXS-NEO trial (co-sponsored by AMGN) just opened for patient recruitment:
Re: CCXI/complement space -
Recently I sold out of IFRX, not because I do not believe in it, just that it is so early on and it went up over 50% from my buy point.
Further on the complement front, today ALXN reported good news on their Soliris replacement.
Re: CFO departures
If the company’s clinical programs succeed the CFO probably won’t get much credit, but if the clinical programs fail the CFO will inevitably share in the taint. So, among all senior officers, the CFO arguably has the most to lose by sticking around when things begin to turn sour.
FPRX CFO “to pursue another opportunity”
Absolutely. 4 of the 9 epacadostat responders were PD-L1 negative. But I didn't try to dive into this because I don't know if they were treatment naive or second line. At that point, I don't know if first line PD-L1- is a harder group than second line PD-L1+ etc... so hard for me to make a useful comparison.
But at this point I'm very skeptical about open label PD-L1 testing results. There can be a fair amount of subjectivity in the test if not done rigourously.
NKTR has 22 evaluable RCC patients with 0 or 1 prior line of therapy and accrued 11 responses (1 CR) in 22 patients, or 50%.
INCY had 19 evaluable patients with 0 or 1 prior line of therapy* and accrued 9 responses (1 CR) for 47%. I don't have exact breakdown of how many were 0 and how many were 1 prior therapy, but the enrollment ratio was 3:4. FWIW, I'm *very* pessimistic in this indication for epacadostat.
ACHN YE17 CC notes -
The curiosity about this announcement is that due to PK potential limitations, ACHN may move forward with one of the other FD inhibitors that are in Ph 1 or close to it. They will try to get a once a day dosing compound to completely block FD and then will run with it. According to management discussions.
(ENTA) Re: MoAs of RSV treatments in development
Most RSV treatments in development, including the one about which you posted, are fusion inhibitors. RSV fusion inhibitors work by preventing viral entry into a host cell, but they don’t work on every at-risk cell. Once a given cell is infected with RSV, a fusion inhibitor cannot stifle the viral activity in that cell, which leaves a residual disease burden that may compromise the overall efficacy of the drug.
ENTA’s EDP-938 is not a fusion inhibitor, but rather an N-protein inhibitor. An N-protein inhibitor disrupts RSV’s viral-replication machinery inside an infected cell in an analogous way to the MoAs of HCV DAAs.
The above is a consequential distinction for ENTA’s RSV program, IMO.
Reviral - positive P2 RSV data
https://www.reviral.co.uk/news/31/48/Positive-results-achieved-in-ReVirals-Phase-IIa-RSV-challenge-study.html
Feb 5, 2018 Positive results achieved in ReViral’s Phase IIa RSV challenge study
ReViral’s RV521 fusion inhibitor produces highly significant reduction in viral load and clinical symptoms
London, UK, 5th February 2018 / ReViral, a UK-based biotech company focused on developing novel compounds targeting respiratory syncytial virus (RSV), today announced successful results from its Phase IIa placebo-controlled challenge trial in healthy adult subjects infected intranasally with respiratory syncytial virus (RSV). The study of RV521, an oral RSV fusion inhibitor, achieved all its primary and secondary endpoints (significantly reduced viral load, reduced total mucus weight and reduced clinical symptoms) compared to placebo.
RSV is a pathogen that infects the human respiratory tract, potentially leading to bronchiolitis and pneumonia. While most (but not all) otherwise healthy people recover from the virus, there is an increased risk of severe disease and death in premature infants, individuals with certain pulmonary conditions, the elderly and those who are immune suppressed. Globally RSV is responsible for more than 30 million infections every year.
"RSV infection in children, the immunocompromised and the elderly causes serious disease and there is a significant unmet medical need for treatment." said John DeVincenzo, MD, Professor of Pediatrics and Professor of Microbiology, Immunology, and Biochemistry, University of Tennessee School of Medicine and Medical Director of the Molecular and Viral Diagnostics Laboratories at Le Bonheur Children's Hospital. “Based on the reductions in RSV viral load and clinical symptoms, as well as the safety profile observed in this adult challenge study, clinical trials in naturally infected patients should now be expedited.”
Efficacy was evaluated in healthy volunteers who had demonstrated RSV infection before treatment. Among 66 subjects (randomised 2:1, RV521 to placebo), RV521 treatment rapidly reduced viral load to undetectable levels. Mean total mucus weight and total symptom diary score (daily reporting of symptoms such as stuffy nose, cough and sore throat) were also significantly lower for RV521 treated patients.
Safety analysis demonstrated no changes in laboratory-determined safety parameters and a balanced adverse event profile between and within both dose groups and placebo. No treatment-related serious adverse events occurred.
Eddy Littler, ReViral CEO, said, “RV521 has shown best in class properties as an RSV therapeutic including efficacy, dose and safety. The company will now move forward to a clinical study in infants”. The full data will be presented at the American Thoracic Society meeting in San Diego (18-23 May, 2018).
IFRX/CCXI -
2. Thanks for pointing out the Innate Pharma asset. I am aware of a complex literature of C5a biology in myeloid cells that have been suggested to play a role in specific oncologies. I view this aspect of C5a and is receptor(s) function as speculative and insufficiently compelling at the current time. Is there a candidate in search of a disease here, or a disease in search of a target? I see that the Innate obtained this C5a antibody asset from Novo, FWIW. One question here (for myeloid derived suppressor cells) is whether C5a is sufficiently upstream to have a major effect.
3.Concerning avacopan to IFX-1 in AAV, the initial IFX-1 data needs to be longer term. The intriguing thing to me about IFX-1 is the apparent longer term effect at reducing C5a levels. I am sure blockade is quick, as avacopan may take a few days to come to steady-state. Is that really all that important? I think not. That is why I go back to the extent of blockade by each approach. The degree of blockade is important tor true remission as it appears that IFRX sees in HS. Speed is only somewhat important. As to indirect off target effects of avacopan, it is true that generally only some 50-500 molecular targets are evaluated in any in vitro drug specificity test. So with any small molecule there is always that theoretical possibility. But animal tox and human work to date should be sufficient, unless some idiosyncratic tox shows up in man. I would be more concerned with low level liver function tests enzyme elevations or phospholipidosis, for that matter. But overall, I am most concerned about the mediocre drug-like physical properties of the CCXI molecule including solubility.
I added significantly to my position this morning, but did not get the low. Choose a horse and run the race to C3G disorders. Factor D or bust I guess.
SGMO -
Sangamo would also receive tiered royalties on sales of potential future products resulting from the collaboration.
IFRX/CCXI -
Not at all. Neutrophil attack and influx is part of the disease pathology and one way to measure efficacy is by measuring the rate of neutrophil decrease. Both drugs decrease neutrophil levels; both drugs seem to be effective. Both drugs have pros and cons. At this point, there is no way to tell which will be the better drug.
IFRX/CCXI -
what is important is the reduction in neutrophil levels driven by each drug and the biological role of that second receptor. Some studies have indicated that C5R2 (aka C5L2) is needed to drive repair and is required to recover from anaphylactic/septic shock. Also, many of these kidney diseases have protein deposits that are damaging. There are reports that Soliris actually increases these deposits as the antibody gets gummed up in the mess. For that reason a small molecule that binds to receptors on neutrophils may have an advantage.
Re: IFRX vs CCXI
I follow the work of each company, and my view is that the difference is in the degreee of blockade of the C5aR by each company in the clinic. I think investors in the biopharma field under-appreciate the extent to which a receptor blocker actually achieves, considering that receptor occupancy is sigmoidal and hence complete blockade is difficult to achieve. It is also of interest that the classical neutrophil C5aR (the originally named CD88 protein) is considered to have a 'hair pin trigger'.
The field of C5a small molecule antagonists has been an active one for many years, with a limited amount of chemical matter having drug like properties having been identified. The CCXI compound is considered 'bricky', with relatively poor drug like properties including solubility. The question to ask CCXI management is to what extent they have C5aR blockade, at both peak and trough blood levels. Also whether the drug hits the second C5a receptor (see below).
As to IFRX, they have some fantastic C5aR biologists that had extensive training in Peter Ward's lab in the Dept of Pathology at the University of Michigan. They appear to have in IFX1 a novel C5 mAb that may block cleavage by the convertase, but also by 'rogue' plasma borne proteases. It is not clear to what extent this may be significant. They have shown compelling activity in HS, though much more needs to be done. My view is inflammatory skin disorders are where the action will be for C5 approaches, as in hydradenitis supportiva, lichen planis and the like.
IFRX vs CCXI
I don't understand how the IFRX approach in complement diseases is better than what CCXI is pursuing with their lead drug avacopan. IFRX is pursuing anti-C5a with an antibody whereas CCXI is taking a more selective approach with a pill in hitting C5aR specifically. See slide 16 of CCXI presentation showing more detail of approach: http://files.shareholder.com/downloads/CCXI/6019127124x0x968844/82BAAA9A-8A2F-4977-9C9C-FF93DF0FC5E9/CCXI_Corporate_Presentation.pdf .
So, what is better about what IFRX is doing? A key point that should be noted is there doesn't seem to be a lot of overlap in disease indications between the two as CCXI is specifically targeting aHUS and C3G whereas IFRX is targeting hidradenitis suppurativa with the lead indication (but also targeting AAV which is lead indication for avacopan).
VXRT—I don't ascribe any material value to AVIR's contributions to the merged company (other than cash). The stock is essentially a call option on VXRT's oral-vaccine technology.
AVIR now trading as VXRT following 1:11 reverse split.
MRTX -
No warts per se, but very early data.
MRTX addendum: Today’s news is the kind of potential I-O breakthrough I was referring to in #msg-132978691 and #msg-133009861.
Jacob replied to your tweet on ARPO. What do you make of it?
POXEL.PA - deal with Roivant for imeglimin
https://www.poxelpharma.com/en_us/investors/news-events/press-releases/detail/86/roivant-and-poxel-announce-strategic-agreement-for
Roivant and Poxel Announce Strategic Agreement for Development and Commercialization of Imeglimin in the U.S., Europe, and Additional Countries Worldwide
FEBRUARY 12, 2018
Poxel to receive upfront payment of $35 million (approximately €28 million), potential future development and regulatory milestone payments and sales-based payments of up to $600 million (approximately €486 million), and double-digit royalties on net sales
Roivant to concurrently invest $15 million (approximately €12 million) in Poxel through subscription to newly-issued ordinary shares at €8.5 per share
Poxel to contribute $25 million (approximately €20 million) to the development program
Roivant will be responsible for imeglimin’s development and commercialization in the U.S., Europe, and other countries outside of Poxel’s partnership with Sumitomo Dainippon Pharma
Poxel to hold investor call today at 1 pm ET (7 pm CET)
BASEL, Switzerland & LYON, France--(BUSINESS WIRE)-- Roivant Sciences, a global healthcare company focused on realizing the full value of promising biomedical research, and POXEL SA (Euronext: POXEL - FR0012432516), a biopharmaceutical company focused on the development of innovative treatments for metabolic disorders including type 2 diabetes, today announced the signing of a strategic development and license agreement for imeglimin, an investigational oral therapy which has been developed by Poxel for the potential treatment of type 2 diabetes, in the U.S., Europe, and all other countries not covered by Poxel’s existing agreement in East and Southeast Asia.1 This partnership enables Roivant to add an innovative late-stage development program to its pipeline and Poxel gains a strategic development and licensing agreement for imeglimin beyond the company’s partnership with Sumitomo Dainippon Pharma.
This press release features multimedia. View the full release here: http://www.businesswire.com/news/home/20180211005061/en/
Under the terms of the agreement, Poxel is entitled to receive an upfront payment of $35 million (approximately €28 million) and Roivant will invest $15 million (approximately €12 million) in Poxel through a subscription to 1,431,399 newly-issued ordinary shares at €8.5 per share. Poxel is entitled to receive potential future development and regulatory milestone payments and sales-based payments of up to $600 million (approximately €486 million) subject to the successful clinical development and commercialization of imeglimin. Furthermore, after launch Poxel will be entitled to double-digit royalties on net sales. Roivant will be responsible for development and commercialization costs and Poxel will contribute $25 million (approximately €20 million) to the development program. The parties will decide on a potential co-promotion prior to commercialization.
“We are very pleased to partner with Roivant, an emerging leader in biopharma with proven commitment to developing innovative therapies in major disease areas. Roivant’s vision complements Poxel’s strategy of bringing novel treatments for type 2 diabetes and other metabolic disorders to patients,” said Thomas Kuhn, CEO of Poxel. “This is a significant milestone for Poxel and for the development of imeglimin in the U.S., Europe, and other countries outside of the Asian markets where we have already partnered with Sumitomo Dainippon Pharma. The imeglimin Phase 3 TIMES type 2 diabetes program in Japan is underway with a target Japanese New Drug Application submission in 2020, and imeglimin is ready to advance into late-stage development in the U.S. and Europe. 2018 will be a transformative year for Poxel as we advance the TIMES program in Japan, collaborate with Roivant on imeglimin, and increase our focus on our earlier-stage pipeline.”
“We are pleased to have reached this agreement with Poxel as we continue our strategy of in-licensing late-stage development candidates in underserved therapeutic areas,” said Vivek Ramaswamy, Founder and CEO of Roivant Sciences. “This agreement represents the beginning of our focus on metabolic diseases and imeglimin, with its compelling and consistent data, will be a cornerstone program. We are looking forward to rapidly advancing its development.”
Activities in 2018 to support initiation of the Phase 3 program will include differentiation studies to confirm imeglimin’s potential in sensitive patient populations, such as those with chronic kidney disease, as well as manufacturing of the drug product for use in the Phase 3 program. The goal is to initiate the Phase 3 program in the U.S. and Europe in 2019.
Imeglimin has completed Phase 1 and Phase 2 development in 18 clinical studies involving over 1,200 subjects with type 2 diabetes in the U.S., Europe, and Japan, and met its primary and secondary endpoints, including a statistically significant decrease of HbA1c and fasting plasma glucose versus placebo, with a favorable side effect profile. For more information about imeglimin clinical studies, please visit www.poxelpharma.com.
Poxel will host an investor conference call today to discuss this partnership at 1 pm Eastern Time (7 pm Central European Time). To participate in the call, please use the dial-in numbers below.
France: +33 (0)1 70 807 153
UK: +44 (0) 20 3107 0289
US: +1 (877) 293 6124
Conference ID: 8391409
A recording of the conference call will be available two hours after the call’s completion for at least 30 days. To access the recording, use the dial-in below.
Replay Number:
US : +1 (855) 859-2056
Outside US: +1 (404) 537-3406
Access code: 8391409
About Imeglimin
Imeglimin is the first clinical candidate in a new chemical class of oral agents called the Glimins by the World Health Organization. Imeglimin has a unique mechanism of action (MOA) that targets mitochondrial bioenergetics and acts on the three key organs which play an important role in the current anti-diabetic treatment paradigm: the liver, muscles, and the pancreas2. Studies conducted to date have suggested potential glucose lowering benefits through increased insulin secretion in response to glucose3, improved insulin sensitivity4, and suppression of gluconeogenesis2. Imeglimin’s MOA also has the potential to prevent endothelial and diastolic dysfunction5,6,7, and to provide protective effects on beta-cell survival and function8. Poxel plans to publish preclinical and clinical data on imeglimin and to present findings at multiple scientific and medical congresses in 2018.
About Poxel SA
Poxel uses its development expertise in metabolism to advance a pipeline of drug candidates focused on the treatment of metabolic disorders, including type 2 diabetes. We have successfully completed our Phase 2 clinical program for our first-in-class lead product, imeglimin, which targets mitochondrial dysfunction, in the U.S., Europe and Japan, and the Phase 3 Trials of IMeglimin for Efficacy and Safety (TIMES) program in Japan is underway. Our second program, PXL770, a direct adenosine monophosphate-activated protein kinase (AMPK) activator, is completing Phase 1 development. Based on this central metabolic role, targeting AMPK offers the opportunity to pursue a wide range of indications to treat chronic metabolic diseases, including diseases that affect the liver, such as non-alcoholic steatohepatitis (NASH). We intend to generate further growth through strategic partnerships and pipeline development. (Euronext: POXEL, www.poxelpharma.com)
Re: Roche's RG7716/(ARPO)
I saw @JacobPlieth make reference generally to ARPO in connection with this news (wasn't clear to me if in positive, negative, or neutral context). Never heard of the company until his tweet today. Turns out this company was spun out of AKBA in 2011. Here's a link to the company presentation: http://ir.aerpio.com/phoenix.zhtml?c=254540&p=irol-presentations .
In short, they are developing a subcutaneous drug (AKB-9778) that they claim is the most potent activator of the Tie-2 pathway (the ultimate goal of RG7716 and similar drugs). AKB-9778 inhibits vascular endothelial protein tyrosine phosphatase (VE-PTP)(separate target in this similar pathway as Ang-2). ARPO claims that VE-PTP inhibition activates Tie2 more robustly than Ang-2 inhibition (seems to be supported by slide 9 of the company presentation).
If you look at slide 13 of the presentation, it shows the Phase 2a data in DME and it shows that AKB-9778 had no effect alone in change in retinal thickness over time versus the effect seen by Lucentis but then they claim the combo does better than Lucentis alone. Seems hard to believe there will be a true combo benefit given AKB-9778 has no effect on its own. They claim in the slide that DME is primarily a VEGF-driven disease so that's why no monotherapy effect. Still don't understand why we should believe there would be a combo benefit if it's primarily a VEGF-driven disease.
Slide 17 shows Phase 2a data in diabetic retinopathy which is the indication they seem to be focused on now. This shows the percentage of patients at 3 months with a 2-step or more improvement in diabetic retinopathy severity score. At 3 months, data showed just 11.4% of patients hit this with AKB-9778 vs. 4.2% in placebo. Seems very small but then they note they expect this benefit to grow over time (Lucentis showed 31-34% at month 12). But, they also note that Lucentis showed a 16-18% improvement at month 3 previously, which is much higher than AKB-9778 data.
So, I don't understand how this drug is supposed to compete in this landscape. There is no VEGF inhibitor associated with AKB-9778 so how will it compete with dual VEGF/Ang-2 drugs (even if VE-PTP is truly a better target than Ang-2). Also, the data doesn't stack up so far relative to VEGF inhibitors alone in either of these indications so not sure what I'm missing (if anything).
Shionogi - deal terms with Roche for flu drug
[Just showing the PR from back in 2016 that details the terms Shionogi received from Roche for this novel flu drug. Shionogi kept full rights in Japan and Taiwan; has certain co-invest rights in the U.S.; and will get royalties elsewhere.]
http://www.shionogi.co.jp/en/company/news/2016/pmrltj0000002mfp-att/e160229.pdf
Shionogi Enters into a License and Collaboration Agreement with Roche for its Anti-Flu Drug, S-033188
Osaka, Japan, February 29, 2016 - Shionogi & Co., Ltd. (Head Office: Osaka; President & CEO: Isao Teshirogi, Ph.D.; hereafter “Shionogi”) today announced that it has entered into a license and collaboration agreement with F. Hoffmann-La Roche Ltd. (Head Office: Basel, Switzerland; CEO: Severin Schwan, L.L.D.; hereafter “Roche”) for the development and commercialization of its oral anti-influenza drug S-033188, discovered by Shionogi.
S-033188 is a cap-dependent endonuclease inhibitor*1, with a novel mechanism of action. It is expected to be a one-time, single-dose therapy for influenza, having the potential to be both more convenient and, with its novel mechanism of action, more effective than existing marketed anti-influenza products, which are neuraminidase inhibitors*2. In October, 2015, S-033188 has been designated for priority review by the Ministry of Health, Labour, and Welfare of Japan, as a “Sakigake fast-track review candidate.” A Phase II study is currently ongoing in Japan, and S-033188 is projected to be launched in Japan in Shionogi’s fiscal year 2017, which ends March 31, 2018.
Under the terms of this agreement, Shionogi will conduct development of S-033188 in collaboration with Roche worldwide, with the exception of Japan and Taiwan which will be retained exclusively by Shionogi. Shionogi received an undisclosed upfront payment from Roche and is also eligible to receive milestone payments upon successful completion of key development and registration milestones, including marketing approval. Roche will have the right to commercialize S-033188 worldwide (excluding Japan and Taiwan), with Shionogi retaining certain co-promotion rights in the US. Shionogi shall be entitled to receive royalties from Roche on S-033188 sales.
Influenza virus causes an acute and severe respiratory tract infection and is prevalent primarily during the winter season. In the elderly and other high risk populations, influenza infection is associated with significant morbidity and mortality. Roche has previous successful experience in the development of treatments for influenza. Through this cooperation, Shionogi’s goal, consistent with its overall mission, is to supply an innovative and effective medicine to patients worldwide suffering from influenza virus infection.
Shionogi/Roche - new experimental flu drug
https://www.wsj.com/articles/experimental-drug-promises-to-kill-the-flu-virus-in-a-day-1518264004
[Not a direct threat to VXRT as not a vaccine.]
Experimental Drug Promises to Kill the Flu Virus in a Day
Even if drug lives up to claim, it likely won’t be available in U.S. until next year at earliest
By Preetika Rana
Feb. 10, 2018 7:00 a.m. ET
As Americans suffer through the worst influenza outbreak in almost a decade, a Japanese drugmaker says it has developed a pill that can kill the virus within a day. But even if the experimental drug lives up to the claim, it likely won’t be available in the U.S. until next year at the earliest.
A late-stage trial on Japanese and American flu patients found that for the people who took the Shionogi & Co. compound, the median time taken to wipe out the virus was 24 hours. That is much quicker than any other flu drug on the market, including Roche AG’s Tamiflu, which the trial showed took three times longer to achieve the same result. Quickly killing the virus could reduce its contagious effects, Shionogi said.
Also, Shionogi’s experimental drug requires only a single dose, while patients need to take two doses of Tamiflu a day, for five days.
Both Shionogi’s compound and Tamiflu take roughly the same amount of time to entirely contain flu symptoms, but Shionogi says its compound provides immediate relief faster.
Scientists at the Japanese company leveraged their work on a blockbuster anti-HIV drug to create the compound, which works differently from existing flu medicines. It blocks the flu virus from hijacking human cellular machinery, Chief Executive Isao Teshirogi said. Switzerland’s Roche has acquired the international license to distribute Shionogi’s experimental drug.
“The data that we’ve seen looks very promising,” said Martin Howell Friede, who leads the World Health Organization’s advisory on vaccines, including for influenza. “This could be a breakthrough in the way that we treat influenza.”
Shionogi said Japan’s drug regulator is fast-tracking its approval and could approve it for use in Japan as early as March. The regulator declined to comment. Roche and Shionogi say they will apply for U.S. approval this summer and Shionogi doesn’t expect a decision until next year.
Other players including Johnson & Johnson , AstraZeneca PLC and a startup backed by Merck & Co. are testing new compounds to treat influenza A, the most common flu strain. Shionogi’s candidate is furthest along and it says the compound can also treat B strains that infect humans too.
The U.S. has been hit by one of the worst flu epidemics in years, and transmissions are now the most intense since a pandemic in 2009.
The first line of defense is vaccination, although vaccines aren’t always effective as sometimes they don’t target all the circulating flu strains. Scientists around the world are seeking to develop a super vaccine to prevent all strains of the flu, but any breakthrough remains at least a decade away.
Less research has gone into developing new drugs to treat the flu once people are infected—only a handful of such treatments exist, including Tamiflu. Part of what makes the virus hard to tackle is that it invades human cells and tricks them into producing viral material instead of human proteins.
Existing drugs allow the virus to hijack cells, working instead to block the viral material from escaping and infecting other cells. Some still escape, so the drugs slow the rate of infection without immediately containing it.
Shionogi scientists began researching a novel flu drug more than a decade ago, shelving almost 2,500 compounds in the process. Then, the 140-year-old Osaka company, which has created blockbuster drugs used to treat HIV and high cholesterol, had a breakthrough.
Shionogi scientists knew from their research that an anti-HIV drug the company had developed with a joint venture of Pfizer Inc. and GlaxoSmithKline Co. worked by blocking a metallic enzyme that HIV uses as a weapon to hijack human cells. They found the flu virus was also exploiting a metallic enzyme.
“So we said, ‘why don’t we build on our HIV knowledge to find a way to treat the flu?’ And we did,” said Takeki Uehara, who led the compound’s development.
A Roche spokesman said the compound proved significantly faster at killing the virus, and that its single-dose requirement was more convenient. He said the compound offered “improved tolerability” for participants over Tamiflu. Shionogi and Roche are in the final stages of conducting a second late-stage global trial.
J&J’s drug division, Janssen, last month began late-stage trials involving one anti-flu compound named pimodivir, which blocks a different enzyme that allows the flu virus to multiply inside the human body, said Brian Woodfall, head of Janssen’s infectious disease development.
Results from an earlier trial demonstrated that pimodivir “significantly decreased viral load over seven days,” a company spokeswoman said. Pimodivir worked better in combination with Tamiflu. J&J will take several years to enroll patients in the trial, the spokeswoman said.
Separately, Janssen is researching a biologic injectable, which AstraZeneca and Merck-backed Visterra Inc. are also developing. These injections act like antidotes, attaching themselves to foreign invaders, such as viruses, and then disabling them, while leaving healthy cells alone.
AstraZeneca’s biologics unit said it is evaluating preliminary results from a mid-stage trial in patients. Future plans depend on the findings. Cambridge, Mass.-based Visterra said it began enrolling hospitalized flu patients in December for a mid-stage trial.
GSK -
It's going to interesting to see this battle heat up. GILD would seem to have the upper hand vs triumeq w a TAF containing FDC. However their FDC was slightly numerically inferior to tivicay + descovy despite hitting non-inferiority, and I am sure GSK is going to make this a point of emphasis w docs. If I were a patient i would probably choose the latter regimen and just take 2 pills once a day, but in the history of HIV i don't think a multiple pill regimen has ever beat out a single pill FDC, but I think in this case it is going to be close. Dolutegravir has the track record and might be perceived by some as marginally better than bictegravir, which could trump the ease of one less pill a day (especially since both regimens are QD)
I don't understand the point underlying that CELG tweet.