Release Date: August 05, 2026
For the complete transcript of the earnings call, please refer to the full earnings call transcript.
Positive Points
- AbCellera Biologics Inc ABCL completed enrollment for the phase 2 study of ABCL-635 in treating hot flashes well ahead of schedule, with a top-line data readout expected very soon.
- The company has secured significant new business development deals, including T-cell engager collaborations with Vertex and Jazz Pharmaceuticals, adding over $110 million in upfront cash.
- AbCellera Biologics Inc (ABCL) maintains a strong liquidity position with over $565 million in cash and equivalents, plus roughly $110 million in committed government funding, providing a runway of at least three years.
- The phase 1 data for ABCL-635 showed robust and sustained target engagement with a clean safety profile, including no perceptible increase in liver enzymes, which could be a key differentiator from existing small molecule treatments.
- The company's T-cell engager platform has matured over five years, now including diverse CD3 binders, co-stimulatory antibodies, and scalable workflows, positioning it as a key asset for strategic partnerships.
- AbCellera Biologics Inc (ABCL) added two experienced independent directors to its board, bringing complementary expertise in oncology, women's health, immunology, and endocrinology.
Negative Points
- AbCellera Biologics Inc (ABCL) reported a net loss of roughly $55 million for Q2 2026, a significant increase from the $35 million loss in the same quarter of 2025.
- Total revenue for the quarter dropped to approximately $4 million, down from $17 million in the prior year quarter, reflecting a decline in partnership revenue.
- The company missed its internal goal of moving another program into IND-enabling activities in the first half of 2026, indicating potential delays in pipeline advancement.
- Research and development expenses increased by approximately $7 million year-over-year, reflecting higher investment in internal programs and putting pressure on the bottom line.
- The upcoming phase 2 data for ABCL-635 carries key scientific risks, including the unresolved question of whether blocking NK3R in the pre-optic nucleus is necessary for efficacy, which could impact the drug's potential.
- The company acknowledged a pronounced placebo response in similar trials, which could affect the perceived efficacy of ABCL-635 in the upcoming readout.
Q & A Highlights
Q: What is your view on a clinically meaningful improvement in VMS severity, and will threshold analysis for VMS frequency data (e.g., proportion of patients with 90% or 100% reduction) be included with the top-line data?
A: Carl Hansen (President and CEO): Success is defined by a clean safety profile, consistent with phase 1 data, and efficacy comparable to approved small molecules. On frequency, we are looking for at least a 20% response relative to placebo, with a reduction of at least 2 hot flashes per day. On severity, we expect it to track with frequency and be comparable to small molecules, though we haven't set a definitive bar. Historically, severity is easier to hit than frequency, so our focus is on the frequency side.
Q: Why not move directly into phase 3 label-enabling studies in cancer indications (e.g., breast cancer or men on androgen deprivation therapy) instead of starting with phase 2 studies?
A: Carl Hansen (President and CEO): Moving first into the oncology patient population, which is significantly different, is the necessary first step before later-stage trials. We expect to initiate this relatively soon as we prepare for the larger study on VMS associated with menopause. There will be a gap between the readout and finalizing the trial setup, so we are sequencing as quickly as possible.
Q: If the upcoming data confirms a clean liver profile for ABCL-635, what are your plans for phase 3 liver monitoring to establish definitive differentiation, and could this capture the first-line non-hormonal market?
A: Carl Hansen (President and CEO): Safety is a key differentiator. Both approved small molecules require liver monitoring, which is inconvenient. We believe this is associated with small molecule metabolism and not expected with an antibody. Phase 1 data showed no perceptible increase in liver enzymes. We will continue monitoring enzyme levels, but scientifically, there is no reason to expect issues. Additionally, the small molecule has a somnolence side effect linked to NK1R binding, while our antibody is entirely specific to NK3R, so we don't expect that. Improved safety and once-monthly dosing are paramount for this product.
Q: Can you discuss the percentage of internal resources dedicated to the TCE platform versus other platforms like GPCR and ion channels?
A: Carl Hansen (President and CEO): Our TCE work is a longstanding effort, with the last 5 years spent building the foundation. Much of that work is now in the bank, giving us extra bandwidth to take on additional programs. There won't be a big change in resource allocation to TCE, but it will shift from building capabilities to executing on them for internal and partner programs. While I don't have a hard number, significantly more effort is on the GPCR and ion channel side, but TCE remains a strong pillar of the pipeline.
Q: Looking at historical data for elinzanetant and fezolinetant, it seems severity may be exposure-driven. How are you thinking about ABCL-635's differentiation with its extended half-life?
A: Carl Hansen (President and CEO): Both severity and frequency are important regulatory endpoints that need to be hit, and they correlate well. Dose escalation of fezolinetant showed improved efficacy in both frequency and severity, with the severity response lasting longer. I would be cautious about speculating too much, but we are anxiously awaiting the data to dig deeper into this.
Q: Without disclosing targets, what technical features are required to create an acceptable therapeutic profile for TCEs in autoimmune diseases, particularly around depth and duration of cell depletion, cytokine release, and repeat dosing?
A: Carl Hansen (President and CEO): You've highlighted the important things for cell depleters in autoimmunity: deep depletion, safety, and tolerability. However, it all depends on the target and the exact application, so without getting into details, I can't give a very detailed answer on that specific question.
Q: What are your expectations for the placebo arm in the phase 2 trial, and what aspects of the trial design are meant to mitigate placebo response?
A: Carl Hansen (President and CEO): All trials have shown a pronounced placebo response, and we expect ours to be in a comparable range. To reduce it, we've implemented good clinical operations, including a period where patients aren't told exactly what numbers are needed before enrollment. We feel confident about execution, but the exact placebo response is a big question we'll know shortly.
Q: Will the phase 2 top-line data be out to 4 weeks in all patients, or will there be data out to 12 weeks in some patients? Also, how are you thinking about the phase 3 target patient population—exclusively non-hormonal alternatives or also refractory to HRT?
A: Carl Hansen (President and CEO): The top-line data will be 4 weeks in all patients, and we won't report data on a subset out to 12 weeks. Historically, there's good follow-through between 4-week and 12-week data. The phase 2 was done with a single dose, so we're getting an effective dose-response curve. For phase 3, it's early to discuss design. At base case, there are over a million women in the US alone who are contraindicated for hormones. Additionally, there's a substantial number of patients with hot flashes from cancer therapy (prostate and breast cancer) where hormones aren't an option, plus those not tolerant to HRT. We'll consider all this once we have the data.
Q: Can you provide additional color on the blinded safety data emerging from the trial, including overall adverse event rates and discontinuation rates?
A: Carl Hansen (President and CEO): We haven't disclosed any safety data beyond what was shared on the last call. There's nothing that has given us pause or damaged our thesis. We'll wait for unblinding to have a close look, but things are on track.
Q: What's your latest take on the debate about whether inhibiting NK3R in the median preoptic nucleus is crucial versus just suppressing the kisspeptin neurons in the infundibular nucleus?
A: Carl Hansen (President and CEO): This is the key remaining scientific risk. Phase 1 data showed profound suppression of testosterone, deeper than small molecules, lasting the entire dosing interval. This reads through to the kisspeptin neurons, which are believed to be the most important. If those are the only neurons that matter, we'd expect
For the complete transcript of the earnings call, please refer to the full earnings call transcript.
This stock alert was generated using automated technology and GuruFocus financial data to provide readers with timely and accurate market reporting. This content was reviewed by GuruFocus editorial team prior to publication. Please send any questions or comments about this story to [email protected].
