AbCellera (ABCL) Q1 2026 Earnings Transcript

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Date

Monday, May 11, 2026 at 5 p.m. ET

Call participants

• President and Chief Executive Officer — Carl L. Hansen
• Chief Medical Officer — Sarah Noonberg
• Chief Financial Officer — Andrew Booth
• Chief Legal and Compliance Officer — Tryn Stimart

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Takeaways

• Cash and equivalents -- Approximately $530 million reported at quarter-end, supplemented by $125 million in available committed government funding.
• Liquidity position -- $531 million held in cash, cash equivalents, and marketable securities, with $655 million total available liquidity including unused government funding.
• Revenue -- $8 million for the quarter, compared to $4 million in the prior year period; both periods primarily driven by research fees.
• Research and development expense -- $47 million for the quarter, an increase of $4 million over the year-ago quarter, reflecting internal program investment.
• Sales, general, and administrative expense -- $12 million, down over 35% from $19 million in the prior year period, largely due to the resolution of intellectual property litigation and team changes supporting the internal pipeline.
• Net loss -- $43 million, a modest improvement versus the $46 million net loss in the year-ago quarter.
• Loss per share -- Reported as a loss of $0.14 per basic and diluted share.
• Operating cash outflow -- $34 million used in operating activities; net cash outflow for the quarter was $30 million.
• Marketable securities investment -- $23 million invested during the quarter, totaling $428 million in short-term marketable securities.
• ABCL-635 clinical advancement -- Initiated Phase II in January based on favorable interim Phase I data; Phase II top-line results expected in Q3.
• Phase I safety summary -- No serious or severe adverse events or liver toxicity observed across single ascending dose cohorts.
• Pharmacokinetics ABCL-635 -- Exhibited dose-proportional, linear PK with an estimated half-life of 24 days, supporting a monthly dosing regimen.
• Target engagement -- Single doses of 300 mg, 600 mg, and 900 mg reduced testosterone 50%-75% for several weeks in men, indicating sustained NK3R antagonism.
• Additional pipeline updates -- ABCL-575 Phase I top-line data expected Q4; two additional programs (ABCL-688, ABCL-386) aim to enter clinical trials by 2027.

Summary

AbCellera Biologics (NASDAQ:ABCL) reported that major infrastructure projects are substantially complete, providing a strong foundation for internal pipeline advancement. Interim Phase I ABCL-635 data demonstrated a favorable safety profile and sustained target engagement biomarker response, enabling initiation of a Phase II trial in vasomotor symptoms. Management highlighted that top-line Phase II efficacy and safety data remain on track for release in Q3, which they assert could be a pivotal catalyst for the program. Capital deployment remains aligned with a strategic shift towards proprietary programs, and recent litigation expenses have declined, further supporting this focus.

• President and CEO Hansen said, "success in the Phase II portion of this study would be highly de-risking for the program."
• Chief Financial Officer Booth stated, "we have sufficient liquidity to fund at least the next three years of pipeline investments."
• Clinical development plans include the selection of a fifth candidate in the first half of the year, pending ongoing internal evaluation.
• The company reported being on track to initiate up to three new clinical-stage programs by 2027, beyond current disclosed assets.

Industry glossary

• NK3R: Neurokinin 3 receptor, a G protein-coupled receptor (GPCR) targeted to mitigate vasomotor symptoms such as menopause-related hot flashes.
• VMS: Vasomotor symptoms, a term for hot flashes and night sweats commonly associated with menopause or hormone-altering therapies.
• KNDy neurons: Specific hypothalamic neurons involved in reproductive hormone regulation and implicated as targets for NK3R antibodies.
• SAD/MAD: "Single ascending dose" (SAD) and "multiple ascending dose" (MAD) clinical study designs to assess safety and pharmacokinetics at increasing dose levels.
• PK/PD: Pharmacokinetics (PK) and pharmacodynamics (PD); PK describes how a drug moves through the body, PD describes the biological effects produced.

Full Conference Call Transcript

Tryn Stimart: Thank you for joining us for AbCellera Biologics Inc.'s First Quarter 2026 Earnings Call. I am Tryn Stimart, AbCellera Biologics Inc.'s Chief Legal and Compliance Officer. Doctor Carl L. Hansen, AbCellera Biologics Inc.'s President and CEO, Doctor Sarah Noonberg, AbCellera Biologics Inc.'s Chief Medical Officer, and Andrew Booth, AbCellera Biologics Inc.'s Chief Financial Officer, are speaking on today's call. During this call, we may make statements about our strategic priorities and financial outlook based on our current expectations and in accordance with the safe harbor provisions of the Private Securities Litigation Reform Act of 1995. Our statements are subject to a number of risks, uncertainties, and other factors that could cause actual results to differ materially from those described.

Please review the Risk Factors section of our most recent Form 10-Ks and subsequent 10-Q filings with the SEC for a more detailed discussion of these risks. AbCellera Biologics Inc. assumes no obligation to update any forward-looking statements to reflect events or circumstances after today's date. Our presentation today, our earnings press release, and our SEC filings are available on our Investor Relations website. The information we provide about our pipeline is intended for the investment community and is not promotional. As we transition to our prepared remarks, please note that this call is being recorded and will be available for replay on our Investor Relations website, and that all dollars referred to during the call are U.S. dollars.

After our prepared remarks, we will open the lines for questions and answers. Now I turn the call over to Carl.

Carl L. Hansen: Thanks, Tryn, and thank you everyone for joining us today. 2026 has the potential to be a big year for AbCellera Biologics Inc. We started the year in a strong financial position, with our platform and large infrastructure projects substantially complete, and with our internal pipeline set up for multiple catalysts over the next 24 months. Our key priorities for the year include delivering top-line data readouts for ABCL-635 and ABCL-575, advancing ABCL-688 and ABCL-386 through IND-enabling activities, and adding at least one new development candidate to our pipeline. In January, on the strength of early biomarker and safety data, we announced that our lead program, ABCL-635, had moved into Phase II testing.

By far, the most important data readout in 2026 will be the top-line readout of this study, anticipated in Q3. On today's call, we are excited to present interim Phase I data for this program. As a reminder, ABCL-635 is a potent antagonist of NK3R, a GPCR target that has been clinically validated for the treatment of vasomotor symptoms, also known as hot flashes. It is the first GPCR-targeting antibody from our platform to advance into clinical testing and is being developed as a potential first-in-class antibody medicine for the non-hormonal treatment of moderate to severe hot flashes associated with menopause. We believe ABCL-635 has potential to address a large need and market opportunity in women's health.

For most women, hot flashes are the most problematic symptoms of menopause. They can be highly disruptive to sleep, to work, and to family life, and present a significant burden that persists for a median of over four years. At any given time, it is estimated that more than 12 million women in the U.S. experience moderate to severe VMS, of which more than 6 million will seek treatment. Menopause hormone therapy, an effective treatment and currently the standard of care, is unsuitable for at least an estimated 20% of these women because of contraindications, tolerability, and other factors.

As a result, we believe there are over 1 million women in the U.S. who could benefit from safe and effective non-hormonal treatments. Assuming only price parity with approved small-molecule NK3R antagonists, we estimate the total addressable U.S. market for non-hormonal VMS treatments to be at least $6 billion annually. From this, we believe there is upside potential in pricing, as well as in broader use by patients who experience VMS caused by cancer treatments that reduce hormone levels. This includes patient populations in breast, ovarian, and prostate cancers.

ABCL-635 aims to provide a treatment option that has efficacy comparable to small molecules, a differentiated safety profile without the need for liver enzyme monitoring, and an advantage in dosing convenience, with once-monthly subcutaneous self-injection. I will now turn the call over to Sarah to present details about the program and our interim Phase I results. Sarah?

Sarah Noonberg: Thank you, Carl. I will now discuss the Phase I data that led us to advance ABCL-635 into Phase II development. The Phase I first-in-human trial was a randomized, double-blind, placebo-controlled, two-part study designed to evaluate the safety, pharmacokinetics, and pharmacodynamics of ABCL-635 in healthy volunteers. In Part A, single ascending doses of ABCL-635 or placebo were evaluated in 40 healthy men and postmenopausal women divided into five cohorts. Each cohort contained eight participants, six randomized to ABCL-635 and two randomized to placebo, and each cohort included both men and women. Participants were administered a single subcutaneous dose of study drug ranging from 30 mg to 900 mg and followed for approximately 20 weeks.

The unblinded data from the single ascending dose portion is available and will be discussed today. In Part B, multiple ascending doses of ABCL-635 or placebo were evaluated in 16 postmenopausal women. Participants received monthly doses of 300 mg or 600 mg every month for three months and then were followed for 20 weeks after the final dose. Data from the multiple ascending dose cohorts are still blinded as the final follow-up visits are still ongoing. This slide outlines key demographic characteristics of our study population in the single ascending dose group. Of the 40 healthy participants, there were 30 participants across five escalating dose cohorts in the total ABCL-635 group and 10 participants in the pooled placebo group.

The study targeted healthy adults between the ages of 40 and 65 with a median age in the mid-50s across treatment and placebo groups. We included both men and postmenopausal women in the study, and while the total ABCL-635 population had a greater percentage of women, the pooled placebo group had a greater percentage of men; it is important to note that every individual cohort included at least two male participants treated with ABCL-635, which is important for evaluating pharmacodynamic endpoints. The vast majority of participants across all cohorts were Caucasian.

Baseline body mass index, or BMI, was consistent across most groups with the exception of the 900 mg group, where we observed a lower median weight and, accordingly, a lower BMI. We do not believe this difference had a meaningful impact on the study's overall conclusion. In terms of safety, across all cohorts, treatment with ABCL-635 was generally well tolerated. To date, there have been no reports of serious adverse events, severe adverse events, or adverse events leading to discontinuation. Notably, we have observed no adverse events of liver toxicity, an important differentiator for this program.

The overall incidence of any adverse event occurring in the study was 50% in both the total ABCL-635 treatment group as well as the pooled placebo group, and the vast majority of reported adverse events were Grade 1. The table displays all adverse events reported in at least two participants over the study period regardless of relationship to study drug. The only potential signal identified was self-limiting headache, specifically clustered in the 900 mg cohort. These events were generally mild in severity, typically occurred within the first one to two days post administration, and resolved without complication. It is noteworthy that there were no adverse events of headache reported in the 100 mg cohort.

Injection-site–related adverse events were infrequent across both treatment groups, and gastrointestinal symptoms such as diarrhea occurred at low frequencies and showed no clear dose dependency or increase over time. In addition, a blinded safety review of the ongoing multiple ascending dose portion of the study suggests no new safety signal. As with the single ascending dose portion, to date, there have been no reports of serious adverse events, severe adverse events, adverse events leading to discontinuation, or liver-related adverse events. Looking a bit closer at liver-related safety, this slide displays liver function laboratory tests over time following treatment with escalating doses of ABCL-635 in the single ascending dose portion of the study.

Overall, mean AST, ALT, and bilirubin values remained stable following administration of ABCL-635 with no dose-dependent findings. The dotted lines on each graph represent the mean upper limit of normal, so these values are very reassuring, as are our blinded reviews of liver function tests in the multiple ascending dose portion of the study. Switching gears to pharmacokinetic data, we see that ABCL-635 exhibited favorable linear pharmacokinetics across doses with overall low variability. As illustrated in the left panel, the systemic exposure of ABCL-635 is approximately dose proportional, providing a predictable profile for dose selection in future studies. The estimated half-life of ABCL-635 is approximately 24 days, which we believe supports a monthly dosing schedule.

The right panel displays the data from our multiple ascending dose portion of the study with 300 mg administered every four weeks. The profile confirms that ABCL-635 behaves consistently upon repeat dosing, and analysis of a 600 mg repeat dose cohort is currently underway. While immunogenicity assays have not yet been run, the overall PK profile and general consistency in observed clearing rates is reassuring. Before moving further, it is worth reviewing the biology of NK3R, particularly in the KNDy neurons located in the hypothalamus. In addition to being centrally involved in the physiology of VMS, KNDy neurons are centrally involved in the regulation of the sex hormones through their effects on pulsatile GnRH secretion.

GnRH then acts on the pituitary to release FSH and LH, which then stimulate estrogen and testosterone release from gonadal tissues. These KNDy neuron functions are mediated by neurokinin B binding to the NK3 receptor. Therefore, the ability to block NKB–NK3 receptor signaling can be measured by evaluating the downstream effects of blocking GnRH release, namely circulating levels of estrogen or testosterone. While measuring testosterone levels in postmenopausal women is challenging due to low and variable levels within and between individuals, measuring testosterone levels in men provides a more stable surrogate marker to evaluate NK3R target engagement of KNDy neurons.

Use of testosterone levels in men was previously validated as a biomarker of NK3R target engagement in the early development of the oral small molecule fezolinetant as part of a Phase I study. The figure on the right, adapted from the 2016 paper, shows dose-dependent testosterone suppression following a single administration of fezolinetant at doses ranging from 12 mg to 180 mg. This data provides a useful benchmark of NK3R target engagement and then, along with subsequent Phase II studies, allows us to evaluate how doses associated with different degrees of NK3R target engagement have translated into efficacy on VMS outcomes.

So the enrollment of men into our single ascending dose study was important for us to address a key scientific question of whether an antibody could access NK3R in the hypothalamus and have an analogous effect on serum testosterone suppression. Importantly, we went into the study with a belief that the region of the hypothalamus where the KNDy neurons are predominantly located, namely the infundibular nucleus, was not fully behind the typical blood–brain barrier, consistent with the function of KNDy neurons in sensing hormone levels from the systemic circulation.

We had seen favorable data in nonhuman primates suggesting that these neurons were accessible to an antibody, but it was important for us to de-risk this scientific question early on in clinical studies. With that background, this slide displays testosterone data over time for single doses of ABCL-635 on the left as compared with data adapted from the published study of fezolinetant on the right. Data in both figures have been transformed to display the placebo-adjusted percent change in testosterone from baseline. This is particularly valuable for the fezolinetant data given the natural diurnal changes in testosterone levels that occur during the course of a 24-hour period.

As seen on the left panel, a single dose of ABCL-635 resulted in sustained, dose-dependent testosterone suppression in men over a four-week period with ultimate recovery to baseline by eight to 12 weeks. By comparison, a single dose of fezolinetant resulted in transient, dose-dependent depression of testosterone over a period of hours with recovery to baseline within 24 hours. It is noteworthy that the approved dose of fezolinetant, 45 mg, was associated with a transient decrease of testosterone to a maximum of 50% of baseline values over several hours. By contrast, doses of 300 mg, 600 mg, and 900 mg of ABCL-635 were associated with sustained reductions of testosterone levels of between 50% to more than 75% for several weeks.

Consistent with these findings of NK3R antagonism in controlling the hypothalamic–pituitary–gonadal axis of testosterone, ABCL-635 demonstrated dose-dependent suppression of the pituitary hormones FSH and LH with clear effects at 300 mg, 600 mg, and 900 mg. Based on these pharmacodynamic data, we feel confident that ABCL-635 is able to reach the KNDy neurons in the infundibular nucleus, and we have addressed an important scientific risk for this program. In conclusion, the unblinded interim data from the single ascending dose cohort demonstrated that ABCL-635 has a favorable tolerability profile, a PK profile that supports monthly subcutaneous dosing, and strong and sustained target engagement that meets or exceeds levels previously published for the approved small molecule fezolinetant.

With these data, we moved quickly to initiate Phase II trials in January. We selected a 600 mg subcutaneous dose administered once because we believe it best approximates exposures of 300 mg at steady-state dosing and could be a feasible loading dose to initiate therapy and potentially maximize early effects on VMS. Our efforts are now focused on executing the Phase II portion of the study in order to evaluate the efficacy of ABCL-635 on the frequency and severity of VMS, which are the same endpoints we would expect to use in late-stage clinical development. The study is a randomized, double-blind, placebo-controlled, multicenter study of approximately 80 patients with moderate to severe VMS.

Overall eligibility criteria were designed to be comparable to what has been published for the approved small molecules during Phase III testing. Participants are randomized 1:1 to receive a single dose of ABCL-635 at 600 mg or a matched placebo. The primary efficacy endpoint is at four weeks, although patients will be followed for an additional eight weeks to evaluate the relationship between drug concentrations and efficacy and to facilitate building a PK/PD model. Following the initial 12-week placebo-controlled treatment period, all participants will have the option to enter an open-label extension where they will receive a 600 mg dose.

The study is enrolling well, and we are currently on track to release top-line efficacy and safety data in Q3 of this year. Following that announcement, we intend to present additional data at medical conferences. We believe success in the Phase II portion of this study would be highly de-risking for the program. As a result, we have already begun planning for next steps, which would include a late-stage clinical development program for ABCL-635 in treating moderate to severe VMS associated with menopause, as well as additional studies to evaluate the potential for ABCL-635 to improve VMS associated with common breast cancer and prostate cancer treatments.

I will now pass the presentation back to Carl for highlights about our broader pipeline and upcoming catalysts. Thank you.

Carl L. Hansen: Obviously, we are more than pleased with the Phase I data for ABCL-635, and we look forward to top-line results for the ongoing Phase II study, which remains on track for Q3. Turning to the broader portfolio, the top-line Phase I readout for our second clinical program, ABCL-575, is expected in Q4 of this year. As previously discussed, ABCL-575 is a potential best-in-class OX40 ligand antagonist. From the outset, our strategy has been only to complete Phase I studies prior to partnering it. At present, we have no plans to develop it past Phase I. Beyond ABCL-635 and ABCL-575, we are on track to have up to three additional clinical-stage programs by 2027.

This includes our two undisclosed programs, ABCL-688 and ABCL-386, both of which we believe are compelling opportunities in large markets. We expect both programs will start clinical development in Phase I studies with a clear path to achieving early proof of concept in patients. We will disclose more information on these programs as they enter clinical studies. Finally, we are working towards selecting our fifth development candidate in the first half of this year. Although we still have work to complete, we are on track to deliver on this goal. I will now hand it over to Andrew to discuss our financials. Andrew?

Andrew Booth: Thanks, Carl. As Carl pointed out, AbCellera Biologics Inc. continues to be in a strong liquidity position with approximately $530 million in cash and equivalents, and with roughly $125 million in available committed government funding to execute on our strategy. We are continuing to execute on our plans with a focus on internal programs and leveraging our process development and clinical manufacturing investments. Looking at revenue and expenses, revenue for the quarter was around $8 million, compared to a total revenue of approximately $4 million in the same quarter of 2025, both periods consisting mostly of research fees.

With respect to research fee revenue and as we have indicated in the past, we expect this to generally trend lower as we focus on our internal pipeline. Our research and development expenses for the quarter were approximately $47 million, approximately $4 million more than last year. This expense reflects the focused investment in our internal programs. In sales, general, and administration, expenses were approximately $12 million compared to roughly $19 million last year. The greater than 35% decrease in SG&A expenses relates to the conclusion of our intellectual property litigation and to changes in teams following the focus on our internal pipeline.

Looking at earnings, we are reporting a net loss of roughly $43 million for the quarter compared to a loss of about $46 million a year earlier. In terms of earnings per share, this result works out to a loss of $0.14 per share on a basic and diluted basis. Turning to cash, operating activities for the first quarter used approximately $34 million in cash and equivalents; excluding marketable securities, and with all other investment activities, it amounted to only $3 million in the quarter. This is consistent with the substantial completion of our large investments in facilities and manufacturing capabilities that finished in 2025.

As a part of our treasury strategy, we have $428 million invested in short-term marketable securities, and our investment activities for the quarter included a $23 million investment in these holdings. Altogether, we finished the quarter with $531 million of cash, cash equivalents, and marketable securities, a $30 million decrease in cash for the quarter. As a reminder, we have received commitments for funding for the advancement of our internal pipeline from the Government of Canada's Strategic Innovation Fund and the Government of British Columbia.

This available capital does not show up on our balance sheet, and with over $530 million in cash and equivalents and the unused portion of our secured government funding, we have approximately $655 million in available liquidity to continue to execute on our strategy. In addition, we have further available liquidity from our ownership of another Vancouver lab-based lab and office building as well as our GMP facility. With respect to the overall company expenditures, our capital needs are very manageable. We continue to believe that we have sufficient liquidity to fund at least the next three years of pipeline investments. With that, we will be happy to take any questions. Operator?

Operator: We will now begin the question and answer session. Please limit yourself to one question and one follow-up. If you would like to ask a question, please press star 1 to raise your hand. To withdraw your question, press star 1 again. We ask that you pick up your handset when asking a question to allow for optimum sound quality. If you are muted locally, please remember to unmute your device. Please stand by while we compile the Q&A roster. Your first question comes from the line of Stephen Willey with Stifel. Stephen, your line is open. Please go ahead.

Stephen Willey: Yeah, good afternoon. Thanks for taking the question, and thanks for providing the granularity here. Just curious as to, you know, as you look at the level of testosterone suppression you are able to achieve with both the 300 mg and 600 mg doses.

I know you talked about maybe there being a loading dose strategy that could be pursued, but I guess I am just interested in, now that you have seen the testosterone suppression and, I guess, what you know about the testosterone as a pharmacodynamic marker in terms of what we have seen from some of the small-molecule antagonists, what is your opinion as to whether or not you think that those drugs are leaving efficacy on the table? And, you know, do you think that a rationale for better efficacy could be potentially displayed in the four-week VMS severity and frequency data? Thanks. And then maybe just a quick follow-up.

As you think about what the next development step for ABCL-635 might be, I know you are talking about this being late-stage development, but do you feel like you will have done a sufficient amount of dose-optimization work to potentially move directly to a Phase III study in 2027?

Carl L. Hansen: Great question, Steve. Carl here. First, I want to highlight that this study is really focused on evaluating target engagement on NK3R in the infundibular nucleus. We think that the biomarker readout reports on that directly, but it is not a direct report on efficacy. So speculating on what the ultimate efficacy will be is difficult to resist, but that is exactly what we are running the Phase II study for and what we are going to know in Q3.

Furthermore, our view—our base TPP and our commercial assessment—is that a winning product, potentially a blockbuster, would be a product that has efficacy that is comparable or equal to the small molecules, a cleaner safety profile without liver monitoring, and a more convenient once-monthly subcutaneous injection. From that perspective, that is the bar. If we see that, or something that supports that in Q3, we are celebrating. We do think that there is a strong scientific case based on the target engagement that we have seen that we might do better, but there is still science that needs to be crossed.

I do not want to get in front of that because that is precisely why we are doing the study and the readout in Q3.

Sarah Noonberg: Hi, Stephen. This is Sarah. I think we will take a look at that proof-of-concept Phase II readout. Part of the reason that we are following subjects for 12 weeks is that we really can build a robust PK/PD model looking at efficacy over time as drug concentrations continue to fall, and that will give us a good sense of how these drug concentrations relate to efficacy. We believe with that data in hand, and with a clear and validated mechanism of action, we have a great position to engage regulators with a late-stage development program.

It may be that regulators want us to test an additional dose in Phase III, which I do not think we would be completely averse to, although I doubt that we are going to need to do that with the data at hand, but that will be a regulatory discussion.

Operator: Your next question comes from the line of Evan Seigerman with BMO Capital Markets. Evan, your line is open. Please go ahead.

Evan Seigerman: Hey, guys. Thank you so much for taking my question. Two for me. One, the testosterone data you shared are obviously very strong. Help us contextualize how this could translate into benefit in patients with VMS. And you had mentioned potentially expanding indications beyond VMS into oncology. How should we think about that potential opportunity? Thank you.

Carl L. Hansen: Evan, this is Carl here. I will start with the first question, then I will hand it off to Sarah. Your question is similar to Steve's. If you look at the published clinical development data from fezolinetant, there is pretty good data to make a correlation between target engagement as measured by suppression of testosterone levels and efficacy. That is data that we have been looking at, and it is one of the reasons we think there is a strong case for increased target engagement giving better efficacy. The caveat is that those experiments are done with small molecules, and so the correlation that is seen with small molecules may or may not translate to an antibody.

That is particularly the case because there is NK3R expressed in another part of the brain that is relevant, the preoptic nucleus, where we do not have a direct read on target engagement. While we are very encouraged, and we believe we are hitting NK3R on the critical neurons, which are the KNDy neurons, there is still scientific risk to cross. As I said to Steve, that is why we are running the Phase II. If that data comes in the way that we would like, then I feel the program is highly de-risked, and then we would be moving quickly to develop further.

I think that is the second part of your question that I will hand off to Sarah.

Sarah Noonberg: Next steps from here, in addition to moving into late-stage development in VMS associated with menopause, we also believe there is considerable upside and value for patients in treating induced menopause associated with various cancer treatments. For breast cancer, this would be treatment with tamoxifen or aromatase inhibitors or oophorectomy, where you have a chemically or surgically induced state of menopause, which can give rise to particularly severe VMS symptoms. In prostate cancer, treatment with androgen deprivation therapy and androgen receptor antagonists and other therapies that decrease hormonal levels similarly give rise to the same symptoms of hot flashes.

We believe—and the oral small molecules have also begun to evaluate this further—that there is benefit for patients beyond those associated with naturally occurring menopause.

Evan Seigerman: Great. Thank you.

Operator: Your next question comes from the line of Srikripa Devarakonda with Truist Securities. Your line is open. Please go ahead.

Srikripa Devarakonda: Hey, guys. Thank you so much for taking my question and congratulations on the data. A couple of questions from me. One, the Phase II dose of 600 mg—you mentioned that it was selected because it approximates the predicted Cmax at steady state for the 300 mg regimen. Just remind us how you came to that decision. More importantly, is there a risk that the single dose of 600 mg fails to maintain the testosterone suppression floor at the end of the four-week window in the Phase II trial? Any risk there? And second, the 600 mg dose seemed to have a lower incidence of headache.

Does this seem a case of small cohorts and not to read too much into it, or given what you have seen with the 900 mg and the 300 mg groups, is 600 mg truly a sweet spot for the tolerability profile?

Sarah Noonberg: Thanks, Kripa, and I appreciate your question. In terms of the durability of effects over four weeks, both our PK data showing a 24-day half-life as well as PD data showing sustained target engagement and testosterone suppression support that four weeks is going to be a good time period to evaluate efficacy. Obviously, the results of the Phase II study will tell us conclusively, as we are measuring VMS every week throughout the 12-week period. In terms of the headache rate that you mentioned, I expect that it is small numbers.

We did not see much in the way of safety findings at 600 mg, although in the 900 mg cohort, it is hard to know if this is a real finding. These events of headache occurred on Day 1 and Day 2, which really is not when you have maximal exposures. Often in a Phase I setting, these are individuals that have not necessarily slept well in a dormitory-like setting, and they are not able to have coffee in the morning, and so headache is often a common adverse event across cohorts in studies. It is also worth noting that in the placebo patient with headache, that was also in the 900 mg cohort.

So it is possible that this is a real safety signal; it is also possible that it is just small numbers. Clearly, our safety at 600 mg is very reassuring.

Carl L. Hansen: I will just add to that if you look at the biomarker data—testosterone, LH, and FSH—all of those show at the 600 mg dose we have robust suppression over the full dosing window. That is approximately the exposure that we would expect at steady state with the 300 mg monthly dose. Three hundred milligrams is also compatible with a commercially available autoinjector at 2 mL. All of those things together have factored into the decision to take the 600 mg forward.

Operator: Your next question comes from the line of Allison Bratzel with Piper Sandler. Allison, your line is open. Please go ahead.

Allison Bratzel: Hey, good afternoon, and thanks for taking the question. Maybe just a follow-up on some of the earlier questions. Could you clarify the rationale for capping the multiple ascending dose trial at 600 mg? Was that based on a ceiling effect on target engagement, or because of the headaches we saw, or just some other reason? And then on the multiple ascending dose data, I think you indicated that remains blinded. Should we expect to see any of that data before the Phase II efficacy readout in Q3, or see that concurrently? What is the status on that?

Sarah Noonberg: Yep, thanks, Allison, for the question. In terms of the 600 mg for the MAD cohort as the top cohort, we selected that mainly because that starts to achieve very high exposures, far beyond what we felt we would need or that would be commercially viable to take forward into late-stage development. This is really to provide a safety window at exposures that we feel are appropriate to take forward, and not because of any safety signals. There was no dose-limiting toxicity that we saw across the study. Regarding your second question, we do not expect to share unblinded MAD data before the Phase II readout.

We can look at blinded safety data, and we really just have the final safety follow-up visit ongoing. We do not expect much to change, although because it is still ongoing, we have not unblinded it. We do not expect to unblind that before the Phase II readout.

Operator: Your next question comes from the line of Brendan Smith with TD Cowen. Brendan, your line is open. Please go ahead.

Brendan Smith: Great, thanks, guys. Thanks for taking the questions, and congrats on the data here. Maybe just to put a pin in this conversation to be sure I am understanding biologically what the goal is here. Looking at the testosterone curves—on slide 12—you are still getting well over 50% reduction at four weeks on that 600 mg dose. Is it fair to say ultimately the goal is to reduce testosterone and then maintain that lower level at a steady state? So the idea being that you would not want to extend that dosing window even longer, potentially, just to make sure that it stays down there? Or is there optionality moving forward to extend to five or six-plus weeks?

Just help us understand the over/under on that. And if I could just quickly follow-up: for the two preclinical assets, 688 and 386, do you have a sense of if one would come before the other in terms of clinical starts, or are they roughly on the same timeframe for 2027?

Sarah Noonberg: I think the goal is prolonged, stable target engagement over the course of the dosing period. We believe that based on the PK, a dosing period of every four weeks is appropriate. Because we are following patients for a full 12 weeks after treatment, we will see if efficacy is maintained beyond that four-week period, which would make us think differently about our dosing regimen. At this point, given the sustained target engagement at 600 mg and what we believe would be associated with 300 mg at steady state, we think that is sufficient for monthly dosing. The Phase II data will tell us more.

Carl L. Hansen: Carl here. They are advancing well. We are not prepared yet to make a call as to which one—ABCL-688 or ABCL-386—is going to meet the clinic first, but we will give you an update on that as things progress.

Operator: Your next question comes from the line of Devanjana Chatterjee with Jones. Devanjana, your line is open. Please go ahead.

Devanjana Chatterjee: Hi, congrats on the data, and thanks for taking my question. I understand that the MAD portion remains blinded and you cannot speak in detail. However, since those are postmenopausal women with or without VMS, I am curious if you have been collecting any kind of PRO data from these women, either in the SAD or the MAD, and if you could speak to any trends of benefit on VMS symptoms that you are seeing? And as a follow-up, in the MAD data you have shared for the 300 mg dose every four weeks, we can see some drug accumulation over time. For the 600 mg, as we think about chronic dosing, what kind of PD impact are you expecting?

Do you think there is room for higher PD engagement, and does it have any implication for the risk–benefit ratio when we think about chronic dosing?

Sarah Noonberg: Although we are treating postmenopausal women and some of them do have VMS, we do not collect efficacy in the multiple ascending dose portion. We do not have the same eligibility criteria, and we are not implementing the diaries that we have saved for the Phase II. We expect a very robust answer from that Phase II in Q3. Regarding PD impact at 600 mg with chronic dosing, the 300 mg, 600 mg, and 900 mg cohorts all show very robust target engagement. With the small number of participants tested, it is hard to say that we would see further target engagement at higher exposures.

When we compare over many weeks to 45 mg of fezolinetant, we feel very comfortable that our degree of target engagement—at least in the KNDy neurons of the infundibular nucleus—is sufficient. We do not believe we will need to go higher. Clearly, steady-state dosing will yield some higher exposures, but that is also why we are thinking about a loading-dose strategy so that we can treat VMS quickly within the first week to two weeks.

Carl L. Hansen: As Sarah mentioned in the prepared remarks, the half-life of the antibody is under a month. Monthly dosing at 300 mg would get an accumulation that starts to approximate what you see after a 600 mg loading dose. That supports starting with a 600 mg dose and then continuing with 300 mg once monthly so that you get to maximum efficacy right away and then hold a steady level through treatment.

Operator: Your next question comes from the line of Steve Seedhouse with Cantor. Steve, your line is open. Please go ahead.

Steve Seedhouse: Good afternoon. Thank you. I wanted to ask about the placebo group and the comparator fezolinetant testosterone experiment. The comparator had some transient reduction in testosterone in the 24-hour follow-up, which you noted is typical diurnal variation. What did you see in the placebo arm of your SAD—was it basically unchanged at steady state? And are you measuring testosterone, given this dynamic, at the same time each day at each measurement, or is it averaged from multiple measures throughout each day? Also, on onset of action: with testosterone basically decreasing throughout the first week post treatment, was that expected? Do you think that is a function of bioavailability at the KNDy neurons in the hypothalamus or something else?

What do these target-engagement kinetics compared to fezolinetant, where the nadir was around eight hours post dosing, tell you about what is going on with the pharmacology here?

Sarah Noonberg: To your timing question, yes, we try to measure testosterone roughly at the same time each day. These are participants coming into the clinic rather than being housed at the clinic, so it is not exact, but morning testosterone at each visit is what we aim for and what we were able to achieve. In terms of the placebo group, we did not do serial measurements over 24 hours in the same way, but with an antibody and with the sustained target engagement that we observed, we did not see any appreciable effects in the placebo group.

Regarding onset, the main difference is the time it takes to get to Cmax with a subcutaneously administered antibody versus an oral small molecule, where Cmax occurs relatively quickly. It is going to take some time for absorption and to reach the site of interest at peak levels. The fezolinetant data show that the linkage between PK and PD is very quick for the small molecule; our kinetics are consistent with subcutaneous antibody absorption and distribution.

Operator: There are no further questions at this time. We will now open the call for closing remarks.

Carl L. Hansen: Thank you, everyone, for joining the call today. We are excited about the progress, and we look forward to updating you in the future. Thanks so much.

Operator: This concludes today's call. Thank you for attending. You may now disconnect.

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