Leadership

Edmund Nesti, PhD

Chief Executive Officer​

Edmund Nesti leads Alcamena with a clear mission: to disrupt drug discovery and unlock the “undruggable” universe. Dr. Nesti’s leadership is focused on addressing large, unmet medical needs by pioneering transformative new therapeutic modalities.​​

Under Dr. Nesti’s direction, Alcamena has developed its Supernatural Peptides™ platform. This platform integrates a GenAI-Guided Directed Evolution engine, which has proven its ability to move assets from target nomination to Investigational New Drug (IND) application-ready status with unprecedented speed. This is validated by the company’s lead program, ASCT-83, which became IND-ready in under 12 months and is now in Phase 1 clinical development.​

​Dr. Nesti’s strategic vision is grounded in deep regulatory and scientific expertise. Dr. Nesti’s background includes experience at the U.S. Food & Drug Administration (FDA) and the Howard Hughes Medical Institute (HHMI). Dr. Nesti’s has personal experience with more than 100 INDs and 6 FDA New Drug Application (NDA) approvals, guiding the team that has collective experience with over 1,000 INDs.​

​Dr. Nesti is now actively seeking partners to accelerate Alcamena’s robust pipeline, specifically for the co-development of ASCT-1124 (IL-6 antagonist) and ASCT-1201 (TNF-α antagonist), to deliver these promising, differentiated therapies to patients worldwide.​

Letter from CEO​

Alex Pisarchik, PhD

Chief Operating Officer and Director of Protein Engineering

Alex Pisarchik is the principal architect of Alcamena’s Supernatural Peptides™ technology engine. He leverages over a decade of protein engineering expertise from industry pioneers like DuPont, Genencor, Arzeda, and ConstructiveBio to drive the company’s scientific operations.​

Dr. Pisarchik led the development of Alcamena’s proprietary DMTA GenAI-guided directed evolution platform. This system, integrating PepFusion™ tunable libraries and the PepGenesis™ AI-design engine, is precisely what enables Alcamena to target the “undruggable” universe, particularly complex protein-protein interactions.​

The power of this platform is validated by Alcamena’s lead asset, ASCT-83, which advanced from target nomination to an IND-ready candidate in under 12 months. Now in Phase 1 clinical development, ASCT-83 has demonstrated a compelling preclinical profile, including:​

  • Potent appetite suppression and significant weight loss in canine models​
  • Robust pH stability (from pH 1-10)​
  • Confirmed oral (PO) and intranasal (IN) delivery potential​
  • Strong neuroregenerative and neuroprotective activity​

Dr. Pisarchik is leading them to apply this same validated, high-speed platform to propel the assets at the center of this co-development proposal—ASCT-1124 (IL-6) and ASCT-1201 (TNF-α)—toward their 12-month IND-enabling milestones.

Noreen Gervasi, MD, PhD

Director of Neurologic Drug Development​

Noreen Gervasi leads Alcamena’s neurologic drug development, leveraging her deep expertise from the National Institutes of Health (NIH) and the Uniformed Services University (USU) to translate complex neuroscience into viable therapeutics.​ Dr. Gervasi’s work is centered on Alcamena’s lead Phase 1 asset, ASCT-83, a first-in-class antagonist targeting the “undruggable” REST:CTDSP1 protein-protein interaction. Her nonclinical development oversight has been pivotal in validating the Supernatural Peptides™ platform by demonstrating ASCT-83’s powerful and diverse activities.​

Under her direction, ASCT-83 has produced a compelling, data-driven preclinical package for its neurological indications, including:​

  • Neuroregeneration: Dose-dependent increase in neurite outgrowth and promotion of neuronal differentiation via the upregulation of key markers (Tuj1/MAP2).​
  • Neuroprotection: Prevention of excitotoxicity and “brain death” in glutamate-injured hippocampal tissue.​
  • Neuropathic Pain: Significant alleviation of mechanical and thermal pain sensitivity in preclinical models.
  • CNS Injury Recovery: Improvement of cognitive and motor function following brain and peripheral nerve injuries.​
  • Neuro-Oncology: Reduction in cell viability across glioblastoma (GBM) cell lines.​

Dr. Gervasi’s work on ASCT-83 has provided the critical in vivo validation for the entire Alcamena platform, de-risking the technology that underpins the ASCT-1124 (IL-6) and ASCT-1201 (TNF-α) co-development programs.

Leon Nesti, MD, PhD

Chief of Clinical and Experimental Medicine​

Leon Nesti brings over 20 years of experience as a U.S. Army orthopaedic hand surgeon and scientist to lead Alcamena’s clinical and translational efforts. Dr. Nesti’s firsthand experience treating trauma-induced pain and neuropathy informs his commitment to developing transformative peptide therapeutics.​

Dr. Nesti’s distinguished career includes combat casualty care at Walter Reed, a postdoctoral fellowship at the NIH, and board certification in hand and upper extremity surgery. Dr. Nesti research on trauma-induced gene expression and progenitor cell activity directly informs Alcamena’s pipeline and platform strategy.​

With deep expertise in regenerative medicine and translational neuroscience, Dr. Nesti bridges clinical insight and scientific innovation to accelerate the development of high-impact therapies for patients worldwide.​

Shawn Chen, MBA

Chief Financial Officer​

Shawn Chen brings over 25 years of financial leadership in government contracting, with deep expertise in growth strategy, operational efficiency, and regulatory compliance. Mr. Chen is the founder of Quantum Consulting Solutions, LLC, where Mr. Chen has advised clients on profitability, accounting systems, and financial health—serving as a trusted liaison with auditors, banks, and regulatory agencies.​

Mr. Chen has held CFO roles at Williams Adley & Co, LLP, Thomas & Herbert Consulting, and System High Corporation, and served as VP of Client Services at NeoSystems Corporation. Mr. Chen experience spans DCAA compliance, incurred cost submissions, and optimizing cash flow and financial systems.​

Mr. Chen earned his MBA from the Foster School of Business at the University of Washington.​

ASCT-83 (CTDSP1:REST Antagonist)

CTDSP1: C-terminal domain small phosphatase 1; REST: RE1 silencing transcription factor

ASCT-83 is a clinical stage first-in-class drug that antagonizes CTDSP1 and REST, which repress neuronal genes1. Prior to ASCT-83, CTDSP1 and REST were considered undruggable because they lack adequate binding pockets for small molecules and are localized in the nucleus, making them inaccessible to antibodies. CTDSP1 and REST are absent or only express at low levels in neurons and pancreatic beta cells (functionally similar to neurons). However, sugary and processed foods, or nerve injury can result in excessive expression in these tissues. High expression levels cause dysglycemia, neuropathy, and in the case in traumatic nerve and brain injury, an incomplete recovery. Additionally, brain cancers, like glioblastoma, have high CTDSP1 and REST levels. The published literature and our data strongly support that antagonizing CTDSP1 and REST improves the outcome of metabolic disorders, nerve injury, and brain cancer2-7.

Important for safety, most REST targets are transcriptionally unresponsive, because the basal organization of chromatin does not permit the epigenetic “writing” of a new set of instructions. However, ASCT-83 mediated-interference of REST chromatin binding in injured or diseased cells permits the re-establishment of durable chromatin state, restoring normal gene expression, thereby addressing the underlying cause of metabolic and/or neurologic symptoms, with a low potential for side effects.

Alcamena has received a “may proceed” letter from the Food and Drug Administration (FDA) to conduct a single and multiple ascending dose study in health human subjects to assess the tolerability and pharmacokinetics of ASCT-83 following daily subcutaneous administration.

Scientific references:

  1. Nesti, E., Corson, G. M., McCleskey, M., Oyer, J. A. & Mandel, G. C-terminal domain small phosphatase 1 and MAP kinase reciprocally control REST stability and neuronal differentiation. Proc Natl Acad Sci U S A 111, E3929-3936 (2014). https://doi.org/10.1073/pnas.1414770111 [pii]10.1073/pnas.1414770111
  2. Uchida, H., Ma, L. & Ueda, H. Epigenetic Gene Silencing Underlies C-Fiber Dysfunctions in Neuropathic Pain. Journal of Neuroscience 30, 4806-4814 (2010). https://doi.org/10.1523/JNEUROSCI.5541-09.2010
  3. Zhang, F. et al. Repressor element 1-silencing transcription factor drives the development of chronic pain states. Pain (2019). https://doi.org/10.1097/j.pain.0000000000001633
  4. Zhang, J., Chen, S. R., Chen, H. & Pan, H. L. RE1-silencing transcription factor controls the acute-to-chronic neuropathic pain transition and Chrm2 receptor gene expression in primary sensory neurons. J Biol Chem 293, 19078-19091 (2018). https://doi.org/10.1074/jbc.RA118.005846
  5. Ueda, H. et al. A mimetic of the mSin3-binding helix of NRSF/REST ameliorates abnormal pain behavior in chronic pain models. Bioorg Med Chem Lett 27, 4705-4709 (2017). https://doi.org/10.1016/j.bmcl.2017.09.006
  6. Conti, L. et al. REST controls self-renewal and tumorigenic competence of human glioblastoma cells. PLoS One 7, e38486 (2012). https://doi.org/10.1371/journal.pone.0038486
  7. Zhang, Y. et al. Comprehensive Analysis of REST/NRSF Gene in Glioma and Its ceRNA Network Identification. Front Med (Lausanne) 8, 739624 (2021). https://doi.org/10.3389/fmed.2021.739624
  8. Martin, D. & Grapin-Botton, A. The Importance of REST for Development and Function of Beta Cells. Front Cell Dev Biol 5, 12 (2017). https://doi.org/10.3389/fcell.2017.00012

ASCT-83 for Obesity & Early T2D​

We target the CTDSP1:REST pathway to unlock the body’s production of BDNF, a potent natural appetite suppressant9, 10.

Obesity & Early T2D​

Appetite Suppressant / Weight loss​
Up to 3x BDNF
28% appetite
9% weight
BDNF 72 h / appetite & weight 1-month​
Model: BDNF human mesenchymal stem cells / appetite & weight in GLP dog study (daily SC administration at human relevant doses) ​

Scientific references:

  1. Xu, B. et al. Brain-derived neurotrophic factor regulates energy balance downstream of melanocortin-4 receptor. Nat Neurosci 6, 736-742 (2003). https://doi.org/10.1038/nn1073
  2. Zuccato, C. et al. Huntingtin interacts with REST/NRSF to modulate the transcription of NRSE-controlled neuronal genes. Nat Genet 35, 76-83 (2003). https://doi.org/10.1038/ng1219​

Treating the Root Cause of Nerve Injury​

Current treatments fail to address the underlying injury-induced repression of neuronal genes by the CTDSP1:REST pathway11-14. ASCT-83 is designed to reverse this repression.​

Neuropathic Pain​

Rapid Pain Reduction​
Up to 70%
In just 1 Week​
Model: Rat spared nerve injury (mechanical & thermal pain)​

Peripheral Nerve Injury​

Motor Function Recovery​
Full Recovery​
In 4 Weeks​
Model: Rat sciatic nerve transection (restored from 40% deficit) ​

Scientific references:

  1. Uchida, H., Ma, L. & Ueda, H. Epigenetic Gene Silencing Underlies C-Fiber Dysfunctions in Neuropathic Pain. Journal of Neuroscience 30, 4806-4814 (2010). https://doi.org/10.1523/JNEUROSCI.5541-09.2010​
  2. Ueda, H. et al. A mimetic of the mSin3-binding helix of NRSF/REST ameliorates abnormal pain behavior in chronic pain models. Bioorg Med Chem Lett 27, 4705-4709 (2017). https://doi.org/10.1016/j.bmcl.2017.09.006​
  3. Zhang, J., Chen, S. R., Chen, H. & Pan, H. L. RE1-silencing transcription factor controls the acute-to-chronic neuropathic pain transition and Chrm2 receptor gene expression in primary sensory neurons. J Biol Chem 293, 19078-19091 (2018). https://doi.org/10.1074/jbc.RA118.005846​
  4. Xiao-Die, X. et al. Increased NRSF/REST in anterior cingulate cortex contributes to diabetes-related neuropathic pain. Biochem Biophys Res Commun 527, 785-790 (2020). https://doi.org/10.1016/j.bbrc.2020.04.106

ASCT-83 for Ischemic Stroke and Traumatic Brain injury (TBI)​

Blocking REST after injury is neuroprotective, prevents brain death, and improves cognitive function​15-19.

Ischemic Stroke & TBI​

60% less brain death
2x anxiety
2x cognitive function​
Brain death at 24 h; anxiety and cognitive function after two weeks of daily treatment at clinically relevant doses followed by a two-week dose free period.​
Model: ​ Brain death assessed in cultured hippocampi glutamate excitotoxicity assay; ​
 anxiety and cognitive function assessed in a controlled cortical impact rat TBI study​

Scientific references:

  1. Noh, K. M. et al. Repressor element-1 silencing transcription factor (REST)-dependent epigenetic remodeling is critical to ischemia-induced neuronal death. Proc Natl Acad Sci U S A 109, E962-971 (2012). https://doi.org/1121568109 [pii]10.1073/pnas.1121568109​
  2. Calderone, A. et al. Ischemic insults derepress the gene silencer REST in neurons destined to die. J Neurosci 23, 2112-2121 (2003). https://doi.org/23/6/2112 [pii]​
  3. Morris-Blanco, K. C. et al. Inhibition of the Epigenetic Regulator REST Ameliorates Ischemic Brain Injury. Mol Neurobiol 56, 2542-2550 (2019). https://doi.org/10.1007/s12035-018-1254-y​
  4. Cheng, Y. et al. Transcription factor network analysis identifies REST/NRSF as an intrinsic regulator of CNS regeneration in mice. Nat Commun 13, 4418 (2022). https://doi.org/10.1038/s41467-022-31960-7​
  5. Liang, H. M. et al. By up-regulating mu- and delta-opioid receptors, neuron-restrictive silencer factor knockdown promotes neurological recovery after ischemia. Oncotarget 8, 101012-101025 (2017). https://doi.org/10.18632/oncotarget.18195

ASCT-83 for Huntington’s Disease​

ASCT-83 reverses the repression of neuronal genes by blocking REST, allowing them to express normally in Huntington’s disease20.
ASCT-83 eliminates nuclear REST​
48 hours post dose​
Model: HEK293 cells administered 500 to 1000 nM of ASCT-83 ​

Scientific references:

  1. Zuccato, C. et al. Widespread disruption of repressor element-1 silencing transcription factor/neuron-restrictive silencer factor occupancy at its target genes in Huntington’s disease. J Neurosci 27, 6972-6983 (2007). https://doi.org/10.1523/JNEUROSCI.4278-06.2007

ASCT-83 for Brain Cancer ​

In brain cancers REST acts as an oncogene by driving cancer progression1. Blocking REST induces cancer cell death and prevents cancer proliferation and migration21.
ASCT-83 kills glioblastoma cells (GBM)
ASCT-83 alone: 85% GBM cell death
ASCT-83 + Temozolomide (TMZ): 100% GBM cell death
ASCT-83 + TMZ: 75% TMZ resistant GBM cell death
Over 4 to 7 weeks​
Model: GBM U87 and GBM temozolomide resistant U251 cells using clinically relevant doses​

Scientific references:

  1. Kamal, M. M. et al. REST regulates oncogenic properties of glioblastoma stem cells. Stem Cells 30, 405-414 (2012). https://doi.org/10.1002/stem.1020
  2. Conti, L. et al. REST controls self-renewal and tumorigenic competence of human glioblastoma cells. PLoS One 7, e38486 (2012). https://doi.org/10.1371/journal.pone.0038486

ASCT-1 (Permeability Enhancer)

ASCT-1 (Permeability Enhancer)

Mechanism: ASCT-1 is engineered to optimize the delivery of small molecules, peptides, antibodies and oligonucleotides.

With high membrane affinity and efficient membrane permeability, it acts as a “molecular doorman”,  facilitating transmembrane passage and improving systemic uptake.

ASCT-1 is designed to improve drug cell and nuclear permeability and overall bioavailability.​

ASCT-1 enhanced antagonist (ASCT-456) efficacy against its nuclear-localized target REST: ​

Increased ASCT-456 REST antagonist activity from 64% to 100%

Increases ASCT-456-induced U87 GBM cell death from 63% to 100%.

Increases ASCT-456-induced U251-TMZ resistant GBM cell death from 0 to 76%

ASCT-1 exhibits no off-target effect on its own.​

48 hours post dose​
Model: HEK293, U87, and U256 cells using clinically relevant doses. ​

ASCT-1124 (IL-6 Antagonist)

Mechanism: A first-in-class topical peptide that binds directly to IL-6, blocking proliferation and inflammation signals. This offers a localized treatment, minimizing systemic side effects.​

ASCT-1124: Reduction and Prevention of Keloid / Hypertrophic Scars ​

ASCT-1124 is a topical peptide that delivers biologic-level potency directly only to the disease site, avoiding systemic toxicity.​

ASCT-1124 dose-dependently decreases proliferation of skin cells (keratinocytes) from 140% with IL-6 alone to zero in the presence of ASCT-1124.

40% reduction in skin thickness, 60% reduction in serum IL-6, and 75% reduction in serum IFN-γ in a humanized IMQ mouse model.​

Keratinocytes 12 hours post dose; humanized mice every 12 hours for 7 days.​
Model: Keratinocytes and imiquimod (IMQ)-induced humanize mouse model using clinically relevant doses. ​

ASCT-1201 (TNF-α Antagonist)

Pathophysiology: In both rheumatoid arthritis (RA) and psoriatic arthritis (PsA), elevated TNF-α in the synovial fluid and tissue causes joint destruction.

ASCT-1201: Refractory Monoarthritis, RA and PsA​

ASCT-1201 is a once-monthly intra-articular (IA) injection that treats only the inflamed joint, eliminating systemic immunosuppression.​

Low nanomolar affinity with no off-target activity.

>40% Reduction in TNF-α signaling in a reporter assay, confirming potent target engagement.​

12 hours post dose​

Model: TNF reporter strain