Xenon Pharmaceuticals (XENE), a Canadian biotech, is quietly developing a pipeline of promising orphan/CNS assets. 2020 is likely to see two phase 2 readouts as well as two trial initiations (one pivotal). XEN1101, a novel Kv7 Potassium Channel Modulator, is being trialed in 300 adult focal epileptic patients with phase 2 data expected in 2H. One can reasonably ascribe a high degree of confidence in phase 2 success based phase 1b data in healthy volunteers and the mechanism of action’s past. XEN007 is being developed for childhood absence epilepsy [CAE]. The drug is already used outside of the US for migraine prevention and vertigo, so we already have a good idea of its safety profile. Additionally, preclinical efficacy data supports its use in absence seizures. On the trial initiation front, XEN469 & XEN901 should move forward in 2020.
Below, I discuss all four of these programs. At the end of 2020 Xenon could reasonably have a pipeline that looks like this:
- XEN496 – a phase 3 asset (enrolling) for pediatric KCNQ2-EE. Highly likely possibility of clinical success based on known efficacy and safety data.
- XEN1101 – a phase 3-ready asset for adult focal seizures (reasonably projected to procure at least $200M in peak annual sales). Highly likely possibility of clinical success based on known efficacy and safety data.
- XEN901 – a phase 2 asset (enrolling) for SCN8A-DEE & adult focal seizures. Reasonably likely to succeed clinically for this condition due to the drug’s specificity for Nav1.6. Additionally, Xenon will be eligible for a pediatric voucher upon FDA-approval (worth upwards of $100M).
- XEN007 – a phase 3-ready asset for childhood absence epilepsy. Reasonably likely to succeed clinically.
XEN496: Pediatric KCNQ2-EE
KCNQ2 epileptic encephalopathy [KCNQ2-EE] is a very rare, genetic epileptic condition that manifests in early infancy and is without FDA-approved therapy.
Epileptic encephalopathies are an epileptic condition characterized by epileptiform abnormalities associated with progressive cerebral dysfunction.
Seizures in these patients are the result of a genetic mutation:
KCNQ2 mutations have been identified in severe neonatal EEs associated with intellectual disability and motor impairment, with a burst–suppression EEG pattern or multifocal epileptiform activity, but also milder forms
KCNQ2 encodes the voltage‐gated potassium channel Kv7.2:
KCNQ2 mediates the “M‐current, a slowly activating, noninactivating potassium conductance that inhibits neuronal excitability.” Mutations in KCNQ2, therefore, cause neuronal excitability, resulting in epilepsy.
- Multiple, daily tonic seizures (“tense muscles”) occurring within the first week of life and lasting up to 1 year, including reports of prenatal seizure activity in utero (“rhythmical jerking or jerking of a limb”). Most patients are seizure-free at age 3.
- Electroencephalograms (EEGs) recording a “burst suppression pattern”.
- Profound intellectual disability; spastic quadriplegia
- Seizures are extremely resistant to current therapies.
These clinical features are very specific to mutations in KCNQ2.
XEN496’s active ingredient is retigabine, aka ezogabine, which had been approved by the FDA in 2011 for adult epilepsies, but was removed from the market in 2017 due to commercial reasons.
Below is a brief history:
The company has stated the withdrawal is for commercial reasons, due to very limited use and declining numbers of patients initiating therapy on the drug.
However, in 2013 the US FDA issued a safety communication and placed a black boxed warning on the drug label, related to risks of retinal abnormalities, potential vision loss, and blue discoloration of the skin, nail, mucous membrane, and white-of-the-eye. Whether these changes were reversible was unknown at that time. The FDA also advised all patients taking the medication to have baseline eye exams, followed by periodic eye exams every 6 months.
The FDA later revised its warning in October 2015. Based on its review of additional safety reports, the FDA decided that the retinal pigment changes associated with the drug did not appear to affect vision, and that the skin discoloration appeared to be cosmetic, without serious side effects. However, at that time the FDA required GSK to do a long-term observational study to provide further information on the medication’s safety, and whether retinal pigment changes associated with its use cause vision loss or other long-term effects.
Potiga can also cause urinary retention. Close monitoring is required in patients with benign prostatic hypertrophy, or cognitive impairment, and also in patients taking anticholinergic medications. Other adverse effects may include QT prolongation; dizziness; somnolence; fatigue; and neuropsychiatric symptoms, including confusion, psychotic symptoms, and hallucinations.
496 specifically modulates Kv7 potassium channels.
Retigabine acts as an activator of neuronally expressed KCNQ‐channels, thereby reducing neuronal excitability. Patients with a KCNQ2‐mediated epileptic encephalopathy may especially benefit from this targeted therapy, as rapid control of seizures could potentially improve developmental outcome.
Xenon believes 496 is an appropriate therapy for this condition:
We believe published case reports where physicians have used ezogabine in infants and young children with KCNQ2 epileptic encephalopathy, or KCNQ2-EE (also known as EIEE7), indicate that XEN496 may be efficacious in this often hard-to-treat pediatric patient population. We have received orphan drug designation, or ODD, from the FDA for XEN496 as a treatment of KCNQ2-EE. After consulting with clinical experts and patient advocacy groups, we submitted a pre-IND briefing package to the FDA that outlined the proposed clinical development plans for XEN496.
KCNQ2 mutations may result in a dominant-negative effect on voltage-gated potassium channels, which in a xenopus model system could be partially reversed by retigabine.
Xenon reports that the FDA will only require one phase 3 trial in ~20 patients:
In response, the FDA indicated that it was acceptable to study XEN496 in infants and children up to 4 years old, and that a single pivotal trial in approximately 20 patients may be considered adequate in order to demonstrate XEN496’s efficacy in KCNQ2-EE.
The company originally intended to initiate a pivotal trial last year but chose, instead, to go forward, first, with an adult PK study after electing to change the drug’s formulation into something that is more kid-friendly (sprinkle capsules). Xenon anticipates filing the IND in the first quarter of 2020. The pivotal trial would, subsequently, be initiated.
This is a product that Xenon, upon approval, could easily market themselves, as I would anticipate quick uptake given the (1) severity and treatment-resistant properties of the condition, (2) complete lack of FDA-approved treatments, and (3) complete lack of treatments under development besides 496.
I will conservatively estimate that there are 2,500 KNCQ2 US & EU patients who would benefit from 496. I will price it at $80,000/year, which is actually conservative compared to other orphan drugs with very limited populations. Assuming a strong penetration (…), this nets $150M/year. I believe there is a high likelihood of success for 496 in this indication (…). Times a multiple of 3, this gives us a current value of $270M.
Reasons for optimism
I believe 496 is a very attractive asset for this particular condition for the following reasons:
- Given the complete lack of treatments, the bar for approval will be fairly low.
- 496 has already procured robust (p<0.001) anti-seizure data in populations less likely to respond to it (adults with focal seizures).
- 496’s mechanism of action should specifically prove beneficial for patients with KNCQ2-EE.
- Given the severity of the condition, I do not believe the historical side effects (cosmetic & urinary retention), associated with the drug’s active ingredient, will outweigh the benefits of seizure reduction and cognitive improvements.
The main risk I see associated with 496 is the possibility of the new formulation acting differently than tablet. Management has indicated, however, that the preclinical studies reveal a very similar profile. The company has already completed the required juvenile toxicology studies for the new formulation.
XEN1101: Adult/Pediatric Focal Seizures & KNCQ2
(…) this second generation Kv7 channel opener is more potent and target‐selective than the first generation Kv7 channel modulator retigabine, which has been shown to be clinically effective in the treatment of focal epilepsy. Retigabine was withdrawn from the market for commercial reasons following black‐box warnings related to discoloration of skin, lips, and nails and retinal pigmentary changes that appear to be related to formation of retigabine‐retigabine dimers. XEN1101 is inactive on Kv7.1 (cardiac Kv LQT1 channel). XEN1101 is a Biopharmaceutics Classification System class 2 small molecule (molecular weight < 400 g/mol) designed to be more potent than retigabine. It is structurally unrelated to XEN901 and any currently marketed AED.
1101 is theorized to have three distinct advantages over retigabine (also, 496):
1. Once-daily dosing (compared to 3x/day)
Studies in nonhuman primates showed a favorable pharmacokinetic profile; for example, a single oral gavage dose of 1 mg/kg resulted in a Cmax of 54.2 ng/mL in male and 68.7 ng/mL in female monkeys, with an elimination half‐life of 10.2 and 8.4 hours, respectively.
2. Lower risk of side effects like pigmentation:
XEN1101 is a metabolically more stable Kv7 opener that cannot form the pigmented dimer and therefore is expected to have improved safety over retigabine.
3. More effective/greater potency at much lower doses:
XEN1101 is effective in several in vivo rodent models of electrically and chemically induced seizures and exhibits a selectivity >100‐fold for Kv7 channels over other ion channels and receptors.
XEN1101 is a Biopharmaceutics Classification System class 2 small molecule (molecular weight < 400 g/mol) designed to be more potent than retigabine. It is structurally unrelated to XEN901 and any currently marketed AED.
1101 was tested in a phase 1 clinical study in 64 healthy volunteers. Xenon assessed the efficacy (via resting motor threshold) and safety of 1101.
Although none of these patients have seizure disorders (“healthy volunteers”), resting motor threshold [RMT] is the minimum stimulus intensity needed to produce a motor response. In epileptic conditions across the board, the resting motor threshold is too low (leaving affected persons far more at risk for seizures). Anti-epileptic drugs work because of their ability, in some way or another, to raise the threshold and, thus, reduce occurrence of seizures.
Although 1101’s mechanism of action is already de-risked a bit because it was formerly FDA-approved for adult focal seizures (retigabine), it is, again, demonstrating its ability to raise the threshold in healthy volunteers, but, this time, at a more robust rate:
Figure 1: 1101 is more effective than retigabine and at lower doses (Source: Xenon Corporate Deck)
On a safety-front, “XEN1101 was well tolerated with typical transient AEs for this class of drugs, eg, mild to moderate drowsiness and dizziness. There were no serious AEs.” Xenon is preparing for a phase 2 study assessing 1101 in adult patients with focal seizures. Additionally, they plan to pursue a 1101 indication in KNCQ2. I suspect 1101 will be a better option for patients with KNCQ2 compared to 496. It will likely replace 496 a few years after 496 hits the market. I believe it was a smart move by management to pursue the rights for an indication in KNCQ2 (its IND supported by GSK granting information) because caregivers/physicians of these patients were utilizing retigabine (aka Potiga) off-label when the product was available a few years ago. So, patients will be able to have access, again, to a Kv7 potassium channel opener that is specifically indicated for the condition. And years later, hopefully, they will have a more effective and safer option in 1101.
Beyond those points, 496 provided the company with a phase 3 ready asset, which is bound to provide value to investors in the shorter-term.
Within the same study, Xenon is conducting a crossover study comparing 1101 to placebo in a double‐blind, randomized, placebo‐controlled study assessing the differences in RMT. The study is expected to be completed later this year.
Xenon is recruiting 300 adult focal seizure patients for a placebo-controlled phase 2 trial assessing 1101 in combination with conventional therapy. Top-line data is expected in the 2H of 2020.
For the same indication, analysts once projected $200M in peak annual sales for ezogabine before it failed commercially, primarily due to safety concerns. I will estimate a 50% chance of success for 1101 in adult focal seizures. Times a multiple of 3 gives us a current value of $300M.
Mechanism of action:
“XEN901 is a potent and highly selective Nav1.6 (voltage‐gated sodium channel type VIII; SCN8A) inhibitor.”
Other sodium-channel anti-epileptic drugs include phenytoin & lacosamide (highly-successful drugs).
- “Mature CNS neurons predominantly express three voltage‐gated sodium channels: Nav1.1 (SCN1A), Nav1.2 (SCN2A), and Nav1.6 (SCN8A).”
- “Nav1.2 and Nav1.6 are both highly expressed in excitatory neurons, and knockdown of Nav1.6 suppresses kainate‐induced seizures in mice. Gain‐of‐function mutations in Nav1.6 have been linked to a severe childhood epileptic encephalopathy (EIEE13), and a selective inhibition of the Nav1.6 channel would directly address the underlying etiology.”
XEN901 is being specifically developed for infantile epileptic encephalopathy-13 (EIEE13), which is the result of a mutation in the SCN8A gene within chromosome 12q13 (hence the #13).
Unlike current anti-epileptic drugs that are nonspecific for sodium channels, 901 is specific for Nav1.6 and, therefore, may be a potent and appropriate option for patients with SCN8A mutations (EIEE13):
Although nonselective sodium channel blockers are widely used as antiseizure drugs, these compounds generally require relatively high plasma concentrations for efficacy and have a low therapeutic index. XEN901 targets a novel binding site in voltage sensor domain IV that enables improved selectivity and hence an improved preclinical safety profile.
XEN901 was evaluated in a modified 6‐Hz electrically induced seizure assay using transgenic mice harboring a patient‐identified SCN8A gain‐of‐function mutation (N1768D+/−). These mice display augmented Nav1.6 currents at the neuronal level and signs of epilepsy including reduced seizure thresholds, spontaneous seizures, and sudden unexpected death in epilepsy. (…) As expected from the relative potency for block of Nav1.6, XEN901 is ~1000 times more potent than phenytoin or carbamazepine in this 6‐Hz assay.
Figure 2: 901 demonstrates >100-fold greater potency compared to current treatments for EIEE13 (Source: Xenon Corporate Deck)
Xenon is currently conducting a phase 1 placebo-controlled, randomized, double-blind trial in healthy volunteers. Interim results (single doses) revealed the following:
- No Severe Adverse Events
- No clinically significant ECG or lab findings (common in drugs similar to 901)
- Mild or moderate adverse effects (most common: headache) that resolved spontaneously
Xenon plans to reveal data in multiple ascending this quarter. Additionally, plans to begin a phase 2 trial in both adult focal seizures and EIEE13 are ongoing, with regulatory submission regarding development in EIEE13 expected by mid-2020.
Adult Focal Seizures
It turns out that Nav1.6 is “the most abundantly expressed isoform in the CNS during adulthood.” Xenon believes this may provide 901 with the therapeutic differentiation needed to put a dent in a large indication like adult focal seizures. This is supported, so far, by phase 1 data:
- “XEN901 was also shown to be greater than 100-fold more potent than phenytoin, carbamazepine and lacosamide in a Maximal Electroshock Seizure model, which is used as a model for focal seizures.”
- “Driven by efficacy at very low plasma and brain concentrations, XEN901 demonstrates an improved therapeutic index over other sodium channel inhibitors in pre-clinical models; the preclinical safety margin for XEN901 is >100 versus <7 for phenytoin, carbamazepine and lacosamide.”
EIEE13 is estimated to present in 50 annual US births. So, the market opportunity for this condition will not be significant. However, it also will not cost much to develop for this indication and Xenon will likely be eligible for a voucher worth upwards of $100M.
It’s estimated that over 3M Americans (~65M worldwide) have active epileptic conditions with 60% of these cases involving focal seizures. ~75% of the cases involve adults. So, obviously this indication is of huge potential. However, 901 will have to provide clear and robust improvements over existing anti-epileptic drugs to have any chance of market success.
Neurocrine Biosciences agreement
Xenon announced in December that they reached an agreement with Neurocrine Biosciences (NBIX) to develop and market 901, along with other prospects:
Neurocrine Biosciences gains an exclusive license to XEN901, a clinical stage selective Nav1.6 sodium channel inhibitor with potential in SCN8A developmental and epileptic encephalopathy (SCN8A-DEE) and other forms of epilepsy, including focal epilepsy. In addition, Neurocrine Biosciences gains an exclusive license to pre-clinical compounds for development, including selective Nav1.6 inhibitors and dual Nav1.2/1.6 inhibitors. The agreement also includes a multi-year research collaboration to discover, identify and develop additional novel Nav1.6 and Nav1.2/1.6 inhibitors.
As a result of the agreement, Xenon secured an upfront payment of $30M. An additional $25M is expected in mid-2020 when Xenon secures an IND for 901.
XEN007: Childhood Absence Epilepsy
Far more prevalent and less serious than other pediatric epilepsies discussed above, childhood absence epilepsy [CAE] is characterized by a profound abruption in consciousness (typically lasting no more than twenty seconds) without impact on body tone. Despite an “absence” of your typical seizure-like symptoms, CAE is associated with changes in EEG.
The EEG appearance of a typical absence seizure (…) consists of generalized 2.5 to 5 Herz (HZ) spike wave discharges (classically, 3 Hz) with abrupt onset and termination (waveform 1). Spike wave discharges are frequently disorganized, and pre- and post-ictal slowing is often present.
Current treatment recommendations include ethosuximide (a T-type calcium channel antagonist used as first-line in CAE) and valproic acid (GABA promotor & sodium channel antagonist used as second-line in CAE).
This recommendation is supported by results of a randomized, double-blind trial that compared the efficacy and tolerability of ethosuximide, valproate, and lamotrigine in 453 children with CAE. After 16 weeks of treatment, ethosuximide and valproate were significantly more effective than lamotrigine (16-week freedom from seizure rates of 53, 58, and 29 percent, respectively), and the rate of drug discontinuation for adverse effects was similar among the three groups. However, valproate was associated with more frequent attentional dysfunction than ethosuximide (49 versus 33 percent). A follow-up study that assessed the same parameters after 12 months of treatment also confirmed that ethosuximide had better efficacy than lamotrigine and fewer side effects than valproate
Most kids respond well to one or the other. CAE typically resolves itself by puberty and is without severe psychosocial consequence in adulthood.
XEN007s active ingredient, flunarizine (calcium entry blocker with calmodulin binding properties and histamine H1 blocking activity), is a marketed drug in Europe, used most frequently for migraine prophylaxis. Xenon believes it is capable of making a difference in CAE, either alone or in combination with one of the two drugs discussed in the paragraph above:
Flunarizine has demonstrated efficacy and preclinical models of absence seizures and flunarizine has been shown to be well tolerated clinically. Flunarizine has significantly reduced the number and duration of spike wave discharges on EEG in these models as monotherapy, and when combined with valproic acid or ethosuximide significantly reduced the spike wave discharge to EEGs more than any drug alone.
Interestingly, usage of many typical antiepileptic drugs are frowned upon in CAE:
Several antiseizure drugs have the potential to aggravate absence seizures in patients with CAE and should be avoided. These include carbamazepine, vigabatrin, gabapentin, and tiagabine. Phenytoin and phenobarbital are known for their ineffectiveness in treating absences and should also be avoided.
All the drugs mentioned above utilize mechanisms of actions involving sodium channels and GABA potentiation.
Preclinical anti-seizure evidence for flunarizine (XEN007)
Calcium channel blockers are agents known to be effective in seizure reduction. 007 would join ethosuximide as the second anti-epileptic agent to primarily work by inhibiting calcium channels:
Preclinical data in flunarizine demonstrate its potential in seizure reduction:
In the present study, flunarizine was also found to reduce the various phases (TF, THLE, CC, PTD, P < 0.001) of MES induced seizures. The significant anticonvulsant effect of flunarizine can be correlated with previous studies which states that the Flunarizine provides a direct neuroprotective effect against the damaging influx of calcium and prevents neural damage. It reduces transmission fluxes of calcium in situation where calcium is stimulated to enter the cell in excess, thus preventing the deleterious consequences of calcium overload within the cell. It readily crosses the blood brain barrier and inhibits entry of calcium into the neurons, primarily under pathophysiological conditions, such as ischemia or seizure activity, without any effect on normal calcium homeostasis. The cerebrovascular effect of flunarizine could provide a direct neuroprotective effect against the damaging influx of calcium and could also prevent neuronal damage as a result of MES induced seizures.
The above, however, must be coupled with a correlation between calcium channels and CAE to be relevant. A literature review clearly suggests a connection between calcium channels (T-type) and absence seizures:
In this review, a broad investigation of recent studies suggests that T-type channels in TC regions (more precisely their propensity for low-threshold burst firing in TC neurons) are the most critical component of SWD generation during absence seizures.
Flunarizine’s ability to inhibit T-type channels is well-documented:
T-channels are low voltage activated (activation threshold of-45 mV), have fast inactivation and slow deactivation. While there are no selective T-type channel agonists, mibefradil, nickel, and flunarizine inhibit these sites.
The evidence above, combined with a plethora of high-quality evidence available online, suggests that XEN007 (flunarizine) has good potential to be a difference maker in CAE.
As management eluded to above, flunarizine’s role in CAE may be in its additive benefit when combined with ethosuximide:
Sodium valproate(…), ethosuximide(…), 200 mg/kg ip and flunarizine (…) 5 or 10 mg/kg ip were first administered independently to rats in order to study their effects on behavioural and EEG aspects of spike and wave discharges (SWDs) induced by y- hydroxybutyrate (GHB,100 mg/kg ip). GHB treated rats show behavioural changes and concomitant repetitive EEG episodes of 7 to 9 Hz SWDs, mimicking human absence seizures (AS), and can be used as a pharmacological model. The number and duration of SWDs were calculated for 1 hr from the EEG and were parameters for drug evaluation. VPA and ESM at 200 mg/kg, significantly reduced SWD number and duration/hr, while FLU showed significant reduction only at 10 but not at 5 mg/kg. Combination of FLU, 10 mg/kg with either VPA or ESM showed significant reduction of SWD number and duration, suggesting an additive effect of the anti-absence agents with the calcium channel blocker, FLU, on experimental absence seizures in rats.
Because the majority of CAE patients respond well to either first- or second-line treatment, the commercial opportunity for an additional drug in this indication is limited. Assuming 007 lives up to its full potential, one could see it being recommended, adjunct to ethosuximide, in the event of inadequate response to ethosuximide alone. As noted above, despite what appears to be a stronger efficacy in CAE for valproic acid, doctors are slow to recommend it due to its side effect profile.
It is estimated that 1/25000 persons (13,000 kids in the US) has CAE. We will settle for 20,000 total US and EU addressable patients. One should assume that the majority of these patients (over 50%) will be properly managed on ethosuximide alone. I will estimate that 25% of CAE patients may be appropriate candidates for 007. Priced at $30K/year, 007s peak annual revenue can be estimated at $150M/year. I believe there is a 40% chance of success for 007 in CAE. Assuming a multiple of 3, this gives us a current value of $180M.
- XEN496 provides Xenon with a late-stage drug in an orphan condition without any FDA-approved drugs. Its active ingredient, ezogabine, is already known to be highly effective in adult focal seizures. The fact that 496 is specific for Kv7 should bode well for an indication in KCNQ2-EE (ezogabine was used off-label for the condition when it was commercially available). Perhaps in a large & chronic (not life-threatening, not “that serious”) indication like adult focal seizures, ezogabine’s side effects were not tolerable (pigmentation changes, urinary retention). Initial fears of vision loss were overblown and, likely, hindered the drug’s commercial chances. Even assuming the same side effects as ezogabine, a serious condition like KCNQ2-EE would happily absorb the negatives if the drug can prove even somewhat effective in this difficult-to-treat condition. But remember, Xenon is working on a pediatric formulation that will aim to prevent ezogabine’s side effects. I believe it is highly likely this asset will prove successful and, if so, will not experience any direct competition.
- XEN1101 will likely follow XEN496 for KCNQ2-EE, due to its enhanced pharmokinetic profile. It also has obvious potential in adult focal seizures – the indication ezogabine achieved & was projected to procure $200M in peak annual sales before safety concerns derailed its commercialization.
- XEN901 is an appropriate candidate for EIEE13, an ultra-rare orphan condition. Its specificity for Nav1.6 may additionally provide therapeutic differentiation over existing therapies for adult focal seizures. The licensing and development agreement with Neurocrine Biosciences provides additional merit to the drug’s potential. It also provides Xenon with non-dilutive funds to drive forth its pipeline.
- XEN007s active ingredient is an already marketed drug in Europe, reducing its safety risk, and has strong preclinical rationale in childhood absence epilepsy, enhancing its efficacy potential. Furthermore, its potential as an add-on therapy to conventional treatments in CAE appears promising and reasonably likely to succeed.
- Xenon will likely have three late-stage candidates by the end of 2020. Xenon is targeting specific orphan conditions with mechanisms of actions that directly address the pathophysiology of these conditions. This is highly predictive of clinical, regulatory, and commercial success. Xenon is also targeting a larger indication in adult focal seizures, in which any of its two drug candidates may provide therapeutic differentiation over existing anti-epileptic drugs.
My price target of $25, achieved before 2021, assumes moderate dilution (I’m projecting $25/share will translate to ~$750M market capitalization. This would involve no more than 20% share dilution) and clinical success in all indications mentioned above.
In the event of acquisition, I would value Xenon between $750M and $900M.
- Any of Xenon’s drug candidates may not prove safe nor effective in any indications (either historical concerns, like eye damage, or newly realized ones).
- Xenon has other clinical assets that may not prove safe nor effective.
- Xenon doesn’t, and may never, produce revenue. Company will likely have to dilute shareholders to fund operations.
- Management may not have been straight-forward and honest about their communications with the FDA and other important regulators.
- Even if Xenon achieves regulatory approval for any of their products, they may not be successful in the market due to a variety of reasons.
- An investment in Xenon may result in a total loss of investment.
- A number of other competitors, currently in development, may arise and provide clinical benefits over Xenon’s drugs that limit Xenon’s potential.
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