Today we announced plans to initiate a Phase 2 trial of our #senolytic drug UBX0101 for patients with osteoarthritis later this year. See below for more details. https://bit.ly/2KgzT4V
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Posted 30 July 2019 - 10:43 PM
Today we announced plans to initiate a Phase 2 trial of our #senolytic drug UBX0101 for patients with osteoarthritis later this year. See below for more details. https://bit.ly/2KgzT4V
Posted 07 August 2019 - 11:20 PM
We announced our Q2 ’19 #financialresults today. Check out the full details here: https://bit.ly/31pBzA4
Posted 09 November 2019 - 06:23 PM
VP of General Medicine Ben Hsu is presenting during the #ACR19 Study Group: Osteoarthritis on Sunday Nov. 10 at 1:00 pm ET. He’ll discuss current #DMOAD in development, including UBX0101, alongside physicians and industry leaders. More details here: https://bit.ly/33JN0nG
Posted 29 May 2020 - 12:00 AM
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Posted 17 August 2020 - 02:15 PM
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P A Y W A L L E D S O U R C E : ENDPOINTNEWS
Edited by Engadin, 17 August 2020 - 02:58 PM.
Posted 17 August 2020 - 10:11 PM
Unity crashed over 65% today given its first clinical trial results.
"Unity said it will narrow its near-term focus to its continuing ophthalmologic and neurologic disease programs, adding that its current resources are sufficient to fund operations well into 2022."
“While these are not the results we had hoped for, the evidence that senescent cells contribute to diseases of aging remains compelling, and we are excited to advance UBX1325 for retinal diseases, which inhibits Bcl-xL, a distinct senolytic target. Diabetic macular edema and diabetic retinopathy are attractive not only because of the strength of underlying biology, but also because of the sensitive, quantitative, and objective clinical assessments available. The burden of senescent cells in various diseases of aging is increasingly evident, which together with our research gives us great conviction in our science and the future of our pipeline.”
The problem with broad-spectrum ageing treatments is precisely this: if you are unable to demonstrate benefit in a clinical indication a whole strategy (senolytics) requires justification.
Posted 18 August 2020 - 10:52 AM
Posted 18 August 2020 - 05:17 PM
Had Unity demonstrate that UBX0101 removed senescent cells in humans? This is obviously an important point.
The results were surprising since I am quite sure Fisetin improved my (undiagnosed) arthritic knee. A number of treatments appear to have helped (elicited from longecity) but with 3 grams of Fisetin the following day the pain increased and the knee weakened this may have persisted for a week or two. But eventually the knee was stronger - I don't notice save the gristling sound - after subsequent Fisetin doses the same response occurred but with a lesser effect - a couple of days the third or fourth protocol it just briefly completely gave way (upon reading this account another poster reported the same symptom after taking Fisetin). This of course wasn't a targeted senolytic and the trial only occurred over 12 weeks. It is possible there will be subsequent benefits a year from now and moreover the pain experienced might in fact have different causes within the two groups.
Given the experience I had with Fisetin it might be reasonable to conjecture that a/ with targeted senolytics the pain induced might last longer b/if I were older (49) the post senolytic symptoms might be more pronounced and the recovery time longer.
Posted 18 August 2020 - 05:14 PM
UNITY Biotechnology is the largest of the handful of biotech startups working on senolytics, therapies capable of selectively destroying a sizable fraction of the senescent cells that accumulate in old tissues. The company entered clinical trials with a first generation senolytic drug quite early in the development of this presently small industry, with so far only the Mayo Clinic and Betterhumans also running trials in humans. This week, UNITY announced the failure of a phase II study for knee osteoarthritis, an outcome that was half expected by some observers and competitors, but which will no doubt prove to be a burden for senolytic companies seeking to raise funds for further development.
UNITY Biotechnology, Inc., a biotechnology company developing therapeutics to extend healthspan by slowing, halting or reversing diseases of aging, today announced the 12-week results from the Phase 2 study of UBX0101, a p53/MDM2 interaction inhibitor, in patients with moderate-to-severe painful osteoarthritis (OA) of the knee. There was no statistically significant difference between any arm of UBX0101 and placebo at the 12-week endpoint for change from baseline in WOMAC-A, an established measurement of pain in OA. Given these results, UNITY does not anticipate progressing UBX0101 into pivotal studies and will narrow the company's near-term focus to its ongoing ophthalmologic and neurologic disease programs.
"Developing novel treatments that selectively eliminate or modulate senescent cells is at the heart of what we do, and we have generated valuable data that will enable us to learn from this study and inform future studies in diseases of aging. While these are not the results we had hoped for, the evidence that senescent cells contribute to diseases of aging remains compelling, and we are excited to advance UBX1325 for retinal diseases, which inhibits Bcl-xL, a distinct senolytic target. Diabetic macular edema and diabetic retinopathy are attractive not only because of the strength of underlying biology, but also because of the sensitive, quantitative, and objective clinical assessments available. The burden of senescent cells in various diseases of aging is increasingly evident, which together with our research gives us great conviction in our science and the future of our pipeline."
It has been a topic for discussion - sometimes quite pointed discussion - in the industry that UNITY adopted a single dose localized injection approach for their delivery of senolytics, delivering their drug to the knee joint directly. Many people have thought that this was a poor choice. On the one hand this means much lower amounts of the drug in question can be used, which is a desirable characteristic when the drug is a toxic chemotherapeutic compound. On the other hand, it is far from clear that the harm done by senescent cells is local to a significant enough degree for this strategy to work. These cells secrete inflammatory and other signals, and much of that is carried throughout the body. If one destroys only half of the senescent cells in the knee joint, does that in fact both meaningfully and reliably alter the character of inflammatory damage, given what is going on in the rest of the body?
There are a few reasons as to why this attempt could have failed. Firstly, the small molecule drug used may just not work reliably enough in humans in comparison to mice. It would be far from the first time that has happened, if so: promising phase I data can evaporate in phase II, just because more and different patients are involved. Mayo Clinic data from the use of the dasatinib and quercetin senolytic combination in patients with idiopathic pulmonary fibrosis suggests that the results, in terms of destruction of senescent cells, are similar in humans and mice, but that is not the drug being used by UNITY, and it targets a different set of mechanisms to induce apoptosis in senescent cells.
Secondly, as noted above, local administration may be a poor strategy if the goal is to reduce inflammatory burden, given that senescent cells throughout the body are capable of contributing to that burden. Maybe it works in some people, but it will be unreliable given the wide variation in status of the systemic inflammatory burden. Unreliability is always a good possibility when trying to explain early success leading to later failure in clinical trials. The Mayo Clinic and Betterhumans trials of the dasatinib and quercetin combination used oral administration, and thus the drug goes everywhere in the body, globally reducing senescent cell counts and the inflammatory signaling that they generate.
Thirdly, the specific mechanism targeted by UNITY may not be as useful as hoped. It is inhibition of the interaction between p53 and MDM, and has the look of something that suppresses or alters the activity of senescent cells as much as destroys them. This can appear good if measuring specific markers of senescent cell signaling, but it might not actually be as helpful as hoped if the cells are still there, and still undertaking activities that are not being measured. The complexity of cell signaling is another point at which mice and humans might differ enough to make a particular type of signaling suppression more effective in one species than another.
Overall, the animal data, and other human data, for the use of senolytics to reverse age-related pathology is compelling. Very compelling. It is unfortunate that the first attempt at bringing an approach to the clinic failed, but numerous other groups are out there working on the problem, and most of them have what look to be better approaches to the challenge. We'll see how the next few trials progress.
Posted 18 August 2020 - 08:05 PM
stock down 20 % haha
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