- NanoString Technologies (NSTG) stock is falling with a bankruptcy filing.
- That comes after it lost patent lawsuits against 10x Genomics.
- The company says it will consider strategic alternatives.
Monday, February 5, 2024
NanoString files for bankruptcy
Cano files for bankruptcy
- Cano Health (CANO) stock is falling following a bankruptcy filing.
- The company has entered into a restructuring agreement with debtholders.
- It plans to continue normal operations throughout the bankruptcy.
Novartis in the lead to acquire cancer drug developer MorphoSys
Drug maker Novartis AG is in advanced talks to acquire MorphoSys AG, a developer of cancer treatments that has a market value of 1.6 billion euros ($1.7 billion), two people familiar with the matter said on Monday.
Novartis has so far prevailed over rival drug maker Incyte Corp, which also made an offer for MorphoSys, the sources said.
The sources added that there is no certainty that the deal negotiations will conclude successfully and requested anonymity because the matter is confidential. They declined to give any information about the acquisition price.
Novartis, MorphoSys and Incyte did not immediately respond to requests for comment.
Headquartered in Planegg, Germany, MorphoSys develops drugs to fight deadly forms of cancers such as myelofibrosis, which is a rare type of bone marrow cancer, and certain types of knotty lymphomas.
MorphoSys main revenue generator is a lymphoma drug called Monjuvi, which it sells as part of a profit-sharing agreement with Incyte. MorphoSys said last week that Monjuvi's U.S. net product sales were $92 million in 2023, and that it expected these sales to come in between $80 million and $95 million in 2024. The company has said it expects revenue to go up as Monjuvi is approved for more indications.
One of MorphoSys' most promising drugs, known as Pelabresib, is an inhibitor of proteins implicated in the development and progression of myelofibrosis.
MorphoSys stumbled in November when Pelabresib missed some key goals in clinical trials, but said it was still planning to apply in 2024 for approval to commercialize the drug in the U.S. and Europe.
To slash costs, MorphoSys shut down some of its early-stage research programs at the start of 2023, laying off about 17% of its workforce. It now employs almost 550 people in its U.S. and German offices, according to the company's website.
Novartis has also been cutting jobs and costs, and spun off its generic drugs business Sandoz last year, part of a focus on fewer therapeutic areas and geographic markets.
Its revenue growth has been driven by its heart failure drug Entresto, its medicine Kesimpta for multiple sclerosis, and breast cancer drug Kisqali.
Revenue gains for Pluvicto, a precision radiotherapy against prostate cancer, eye drug Lucentis and gene therapy Zolgensma against spinal muscular atrophy fell short of market expectations in the fourth quarter of 2023.
https://news.yahoo.com/exclusive-novartis-lead-acquire-cancer-152919282.html
4D Molecular: Positive Interim Data from Phase 2 Wet AMD Trial
- 51 wet AMD patients with severe disease activity (mean of 442 µm central subfield thickness & presence of retinal fluid) and high treatment burden (mean of 10 anti-VEGF injections in preceding 12 months) were randomized to high (3E10 vg/eye) or low (1E10 vg/eye) dose 4D-150 or aflibercept control regimen
- 4D-150 was well tolerated with a favorable safety profile when evaluated through up to 48 weeks of follow-up: no significant inflammation observed (including no Grade ≥1+ inflammation in high dose patients) and all patients remained off topical steroids
- High dose 4D-150 resulted in an 89% reduction in the annualized anti-VEGF injection rate; 84% of patients received 0 or 1 injection, and 63% were injection-free through 24 weeks; visual acuity & central subfield thickness were both stable vs. aflibercept
- Positive interim results enable rapid advancement towards pivotal development, with Phase 3 clinical trial initiation expected in Q1 2025
- Company to host webcast on Monday, February 5, 2024 at 8:00 a.m. ET
Corporate Webcast Details to Discuss the Results:
| Title: | 4D-150 Randomized Phase 2 Dose Expansion in Severe Disease Activity Wet AMD with High Treatment Burden: Interim Clinical Data & Program Update |
| Date/Time: | Monday, February 5, 2024 at 8:00 a.m. ET |
| Registration: | Link |
An archived copy of the webcast will be available for up to one year by visiting the “Investors & Media” section of the 4DMT website at the following link: https://ir.4dmoleculartherapeutics.com/events.
Sunday, February 4, 2024
EyePoint: Topline Data in Phase 2 AMD Trial
- Subgroup analyses underscore favorable clinical profile and durability of EYP-1901
- Presentations highlight previously reported positive Phase 2 DAVIO 2 topline results showing all primary and secondary endpoints were met
- Results presented today at the Angiogenesis, Exudation, and Degeneration 2024 Virtual Meeting
Pliant: Positive Safety, Efficacy Data in Phase 2a Trial in Sclerosing Cholangitis, Liver Fibrosis
- Bexotegrast (PLN-74809) at 320 mg was well tolerated over 12 weeks of treatment with no drug-related severe or serious adverse events; No safety concerns identified across all dose cohorts
- Bexotegrast at 320 mg reduced liver fibrosis markers ELF and PRO-C3 and showed improvements in hepatocyte function and bile flow by contrast MRI imaging relative to placebo at Week 12
- The 320 mg data continue to demonstrate antifibrotic effects of bexotegrast, consistent with previous findings
- Company to host webcast and conference call tomorrow, Monday, February 5 at 8:00 a.m. ET
The Company will host a conference call and webcast with a slide presentation tomorrow, Monday, February 5, 2024, at 8:00 a.m. ET | 5:00 a.m. PT to discuss this update. Members of Pliant’s management team will be joined by Gideon Hirshfield, FRCP, Ph.D., Lily and Terry Horner Chair in Autoimmune Liver Disease at the University of Toronto. Interested parties may access the live webcast on Pliant’s website at Pliant Therapeutics INTEGRIS-PSC Webcast or may participate via telephone by registering in advance at the following link: Pliant Therapeutics INTEGRIS-PSC Conference Call. Upon registration, all telephone participants will receive the dial-in number along and a unique passcode to access the call. An archived replay of the webcast will be available on Pliant’s website for 60 days following completion of the event.
Neuroinflammation: The Natural Next Alzheimer’s Target?
Alois Alzheimer recognized more than a century ago the role of neuroinflammation in the development of the disease that would bear his name.
“If you actually go back to his original drawings, he was drawing the cells, which today we know are microglia,” immune cells of the brain, said Bruce Lamb, executive director of the Paul and Carole Stark Neurosciences Research Institute at Indiana University School of Medicine and co-founder of Monument Biosciences, which is exploring neuroinflammation-targeted Alzheimer’s treatments. “So, he recognized way back, 120 years ago, that these cells were there” and that they could be playing a role in the disease process.
Several studies have established a link between neuroinflammation and Alzheimer’s disease, and the culprit indeed appears to be microglia. “I think it’s very clear that, at least the minute amyloid is deposited in the brain and maybe even before, there’s a microglial response,” Lamb told BioSpace. And it’s this immune response that could be causing problems with neuronal function.
Lamb said that over the last decade and a half, there has been a renewed interest in the role of microglia in Alzheimer’s, spurred in part by discoveries in the genetics of late-onset Alzheimer’s disease. Genome-wide association studies and the identification of rare mutations that occur in families have led to a list of Alzheimer’s-associated genes, and most of these are expressed in microglia, Lamb said.
Meanwhile, transcriptomics, proteomics and metabolomics data from human cases and controls have revealed similar findings, he added. “A lot of the networks and pathways that are disturbed, especially in late-onset Alzheimer’s disease, are in these inflammatory networks.”
Targeting TREM2 and More
Working under the hypothesis that neuroinflammation contributes to the Alzheimer’s disease process, biotech companies are exploring different targets. Vigil Neuroscience is developing a candidate based on the role of TREM2-mediated microglial dysregulation in the disease process. Also targeting TREM2 is Alector Therapeutics, which describes its strategy as immuno-neurology.
TREM2 is expressed on microglia in the brain, but it is really only expressed in response to amyloid deposits, Lamb explained. There is a signaling cascade downstream of TREM2 within the microglia, “and a lot of the other genes that are implicated in Alzheimer’s disease are also in microglia downstream of TREM2,” he said. At his own company, Lamb added, the team is initially targeting the PLCG2 and INPP5D genes, both of which are downstream of TREM2 and also have genetic associations with Alzheimer’s disease.
Boston–based Cerevance is targeting a different gene, KCNK13, which is specific to and upregulated in the microglia. While others are also going after the NOD-like receptor protein 3 (NLRP3) inflammasome, Cerevance is looking to regulate inflammation only in the central nervous system, leaving peripheral immune cells ready and able to fight opportunistic infections, said CEO Craig Thompson. This is particularly important in Alzheimer’s, he added, because the patients tend to be older and frail. “Our thought was, is there a way to damped down the inflammation on the inflammasome but still [leave] other aspects of the NLRP3 that are helpful for normal immune system functioning?”
In preclinical models, the company’s KCNK13-targeting asset, CVN293, had minimal impact on the peripheral immune system while reducing neuroinflammation in the brain, Thompson explained. Cerevance has shown that “we can tamp down the inflammation response, or the inflammasome, but keep all the other surveillance and other aspects of microglia still functioning as they should.” The company is now conducting a Phase I study of CVN293, with topline data expected in the second quarter of 2024.
In Ohio, biotech NeuroTherapia was co-founded by anesthesiologist Mohamed Naguib, who found that microglia upregulated the cannabinoid type 2 (CB2) receptor, CEO Tony Giordano relayed in an interview with BioSpace.
Naguib further found that “CB2 agonists were able to shift the microglia . . . from a proinflammatory phenotype to an anti-inflammatory phenotype,” which improved amyloid clearance and neuronal function in preclinical models, Giordano said. NeuroTherapia is developing a CB2 receptor agonist for Alzheimer’s disease called NTRX-07, which Giordano expects to enter Phase II trials in the third quarter of this year.
“We believe that it’s the continued activation of the microglia and the production of the proinflammatory cytokines that starts to interfere with synaptic transmission and neuronal function,” Giordano explained. “Fortunately, it appears that if you can stop that activity, you’re going to get improvement in neuronal function.”
A Multipronged Attack
Ultimately, Giordano and Thompson agreed that treating Alzheimer’s disease will require a multifaceted attack.
“Alzheimer’s is a very, very complex disease, and you’re not going to treat it with a single agent,” Giordano said. “It’s likely that you’re going to put together a cocktail and we really believe that neuroinflammatory inhibitors are going to be a part of that cocktail.”
Thompson called Alzheimer’s “more of a constellation of diseases” and said that tackling it from multiple approaches will be “really important.” He teased that Cerevance is also looking at other approaches with some of its earlier compounds. While he wouldn’t reveal the targets, he said that, like KCNK13, “they’re very novel approaches.”
Lamb added that anti-amyloid antibodies, including Eisai and Biogen’s Leqembi, appear to be working primarily through the microglia. “The microglia have these FC receptors which bind to the antibodies and then can actually remove amyloid from the brain,” he said.
Amyloid-related imaging abnormalities (ARIA) has been the primary smudge on the surface of drugs like Leqembi and Eli Lilly’s donanemab. Lamb explained that this side effect is thought to be an inflammatory process. “We think it’s amyloid binding to blood vessels where there’s amyloid and that that is actually recruiting immune cells and leading to where there’s an immune dysfunction.” Accordingly, he said, there is a lot of interest in combination therapies with monoclonal antibodies and drugs targeting microglia “to either improve the removal of amyloid, or even better, prevent some of these side effects that are seen with these antibodies.”
When asked which approach is most likely to lead to the next Alzheimer’s breakthrough, Lamb acknowledged he is biased, but said, “I certainly think the immune pathways . . . are near the front of that sort of discussion.”
https://www.biospace.com/article/neuroinflammation-the-natural-next-alzheimer-s-target-/
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