OTC: APTN

Under the JOBS Act, emerging growth companies
can also delay adopting new or revised accounting standards until such time as those standards apply to private companies. We have elected
to avail ourselves of this provision of the JOBS Act. As a result, we will not be subject to new or revised accounting standards at the
same time as other public companies that are not emerging growth companies. Therefore, our consolidated financial statements may not
be comparable to those of companies that comply with new or revised accounting pronouncements as of public company effective dates.

We are also a “smaller reporting company”
as defined in the Exchange Act. We may continue to be a “smaller reporting company” even after we are no longer an emerging
growth company. We may take advantage of certain of the scaled disclosures available to smaller reporting companies and will be able
to take advantage of these scaled disclosures for so long as our voting and non-voting Common Stock held by non-affiliates is less than
$250 million measured on the last business day of our second fiscal quarter, or our annual revenues is less than $100 million during
the most recently completed fiscal year and our voting and non-voting Common Stock held by non-affiliates is less than $700 million measured
on the last business day of our second fiscal quarter.

The Merger

On February 11, 2025, Adaptin Bio, Inc. completed
the business combination contemplated by that certain Agreement and Plan of Merger and Reorganization, dated as of February 11, 2025,
by and among Unite Acquisition 1 Corp. (“Unite Acquisition”), a public shell company incorporated in the State of Delaware
on March 10, 2022, its wholly-owned subsidiary, Adaptin Acquisition Co., a Delaware corporation formed in the State of Delaware on January
30, 2025 (“Merger Sub”), and Adaptin Bio Operating Corporation (formerly “Adaptin Bio, Inc.”) (the “Merger”).
Upon the completion of the Merger, Unite Acquisition changed its name to “Adaptin Bio, Inc.”

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Business Overview

We are a biopharmaceutical company pioneering
a transformational approach to enhance the transfer of therapeutics into the brain, facilitating the treatment of brain cancers and other
unmet medical conditions. The Company’s proprietary technology harnesses the human immune system’s ability to target, recognize,
destroy or deliver therapeutics to specific cells, including cancer cells. Our mission is to be the global leader and pioneer of this
new treatment paradigm, integrating recombinant technology, gene therapy and cell therapy to address the challenges of targeting and
delivering effective therapies, including to the brain for cancer and other central nervous system (“CNS”) indications.

The cause(s), or etiology, of many diseases can
be addressed in part through manipulation of engineered cells. We view targeted manipulation of the human immune system, together with
recombinant technology and/or gene therapy, as a therapeutically disruptive transformation in the way we treat brain and other diseases.
Our lead product candidate has been recently accepted under an investigator-led Investigational New Drug application (“IND”)
to begin first-in-human studies in brain cancer. Assuming success of those studies, our experienced group of scientists and business
leaders intend to develop our proprietary in vivo and ex vivo technology platforms to revolutionize treatment across a
broad array of other therapeutic areas with unmet treatment needs, including CNS disorders, autoimmune disease and cardiovascular diseases,
among others. Pursuing other therapeutic areas will likely require us to either raise a significant amount of additional capital or to
engage in strategic transactions such as spin-offs or out-licenses. Our goal is to initiate preclinical studies on additional product
candidates in 2027, if not earlier.

Our novel technology was originally developed
by researchers in the Department of Neurosurgery at Duke University, led by Dr. John H. Sampson, the prior Robert H. and Gloria Wilkins
Distinguished Professor and Chair of the Department of Neurosurgery and currently the Dean and Vice Chancellor at the University of Colorado
School of Medicine. The group recognized that adoptive transfer of specifically activated functional human immune cells significantly
increases the “hitchhiking” and intracerebral accumulation of macromolecules that are bound to their surface. While circulating
naïve T cells do not typically penetrate the CNS, activated T cells are known to traffic frequently past the blood brain barrier
(“BBB”) and perform routine immune surveillance in the CNS. Adaptin and its collaborators at Duke University are taking advantage
of this CNS trafficking to enhance the localization of macromolecules and other agents to the CNS for cancer and other CNS disorders.

We are closely working with researchers at Duke
University to translate preclinical proof of concept data of its first proprietary platform technology called BRiTE (Brain Bispecific
T-cell Engager) into human clinical trials. BRiTE focuses on the transport of difficult to deliver T cell targeting agents to tumor tissue,
including in the immunoprivileged brain and overcoming the challenges with other immunotherapeutic approaches. BRiTE is a translatable
method to specifically target malignant glioma using a tumor-specific, fully human bispecific antibody that redirects patients’
own T cells to recognize and destroy tumor cells.

The first application of our technology is APTN-101,
a proprietary epidermal growth factor receptor variant III, or EGFRVIII, BRiTE in order to eliminate malignant glioma tumors in a variety
of aggressive preclinical tumor models where the tumor is implanted behind the BBB in the CNS (i.e., orthotopic). We designed APTN-101
to specifically redirect T cells against tumors expressing a well-characterized, mutated form of epidermal growth factor receptors (“EGFRs”)
known as EGFRVIII, on a number of tumor types, including glioblastoma, breast and lung cancer. Because EGFRVIII is exclusively expressed
on tumor cells, but not normal healthy cells, we believe it represents an ideal target for immunotherapy. We have made significant progress
towards first-in-human clinical studies, including:

● A pre-IND meeting with the
FDA outlining a clear path to filing an IND;

● Completion of single-dose IND-enabling
preclinical studies;

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● Submission in April 2023 of
an IND for an investigator-initiated, single-dose clinical trial, and its acceptance in May 2023 by the FDA; and

●

Manufacturing
of APTN-101 in more than sufficient quantities for Phase 1 trials.

● Submission in August 2025 of an IND amendment to include
multiple dosing for the investigator-initiated, multi-dose clinical trial, and its acceptance in October 2025 by the FDA; and

●
Received both internal and external Institutional Review Board (IRB) approval for the investigator-initiated, multi-dose clinical trial evaluating APTN-101 in the treatment of glioblastoma multiforme (GBM) in March 2026.

We also expect to expand our proprietary platform
to other targets and indications. The Company is exploring several external opportunities to continue to advance and expand the product
pipeline.

Strategy

Our goal is to become a leading biopharmaceutical
company focused on the transfer of drugs across barriers and to targeted tissues, including the brain and CNS, to transform current treatment
paradigms for patients and address unmet medical needs. The critical components of our strategy are as follows:

● Advance the development
of APTN-101 for the treatment of glioblastoma. The FDA’s acceptance in May 2023 of the IND for APTN-101
and the acceptance in October 2025 of the amended IND for APTN-101 for the multi-dose first-in-human clinical trial in glioblastoma patients.

● Advance preclinical development
of APTN-101 to support one or more additional INDs for additional kinds of cancer. We have designed APTN-101
to incorporate EGFRvIII, which is expressed on a number of tumor types, including breast and lung cancer (with or without brain metastases),
so we are considering pre-clinical work to support INDs for these indications to be filed.

● Design and advance other
early-stage drug product candidates for undisclosed rare and unmet needs. Because our proprietary technology
enables drugs to cross barriers and target tissues, including the brain, we believe it has numerous potential applications in areas of
unmet medical need. We are evaluating which of those indications would be most strategic to pursue in the near-term.

● Acquire, in-license or
develop complementary delivery technologies that will allow us to produce BRiTE compounds or manipulate and activate immune cells in
vivo. We continually evaluate technologies that will further enhance therapeutic effect, improve safety and manufacturability,
or reduce costs of our products.

● Acquire targeted clinical
compounds for conditions with unmet needs where our technology could be transformative. We continually evaluate development and
in-licensing opportunities and may acquire clinical compounds for conditions with unmet medical needs where our technology’s ability
to cross barriers and target specific tissues, including the brain, could be transformative of the treatment paradigm.

● Pursue a capital-efficient
commercialization strategy. For products with smaller and/or orphan patient populations, our plan is to build an infrastructure
to commercialize our drug products within the United Sates. Drawing upon our experience in commercializing specialty pharmaceutical products,
we aim to build a specialized yet efficient infrastructure that will support the entire commercialization continuum, including stakeholder
education, treatment decision and initiation, and product access throughout the patient journey. In addition, we plan to seek established
companies to commercialize our drug products for larger addressable markets and outside of the United States.

● Leverage, protect and
enhance our intellectual property portfolio and secure patents for additional products and indications. We intend to expand our
intellectual property, grounded in securing composition of matter and method of use patents for new products and indications. We plan
to enhance the intellectual property portfolio further through learnings from ongoing preclinical studies, clinical trials and manufacturing
processes.

● Outsource capital-intensive
operations. We plan to continue to outsource capital-intensive operations, including most clinical development and all manufacturing
operations of our product candidates, and to facilitate the rapid development of our pipeline by using high quality specialist vendors
and consultants in a capital efficient manner.

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Glioblastoma

Background

Glioblastoma multiforme (“GBM”),
the highest grade (World Health Organization (“WHO”) grade IV) astrocytoma, is the most common and malignant brain tumor,
accounting for about 50% of all gliomas and 12%-15% of all brain tumors. GBM tumor cells, which arise from stem cells or immature astrocytes
due to genetic abnormalities, grow rapidly and disseminate in the brain. In addition, GBM cells can invade the intracranial blood vessels
to areas away from the tumor core.

Although glioblastoma can happen anywhere in
the brain, it usually forms in the frontal lobe and the temporal lobe. Glioblastoma rarely occurs in the brain stem or spinal cord. As
glioblastoma grows, it spreads into the surrounding brain. This makes it difficult to remove the entire tumor with surgery. Although
radiation therapy and chemotherapy can reach the tumors, glioblastoma cells can survive and regrow. Glioblastoma is very challenging
to treat due to tumor-specific features, such as its rapid growth rate, the poor function of the immune system cells within the tumor,
and inherent resistance of the tumor cells to many types of treatments.

There is no direct risk factor associated with
most cases of glioblastoma. Certain rare genetic diseases, such as Li-Fraumeni and Lynch syndrome, are associated with gliomas. However,
these affect only a small portion of patients with glioblastoma. Besides genetic syndromes, the only well-established risk factor is
prior exposure to ionizing radiation that is used to treat certain head and neck cancers.

Brain tumor symptoms vary and depend on the tumor
location. The most common glioblastoma symptoms are headaches, seizures, and progressively worsening numbness or weakness. Headaches
with red flag symptoms warrant a trip to the doctor for a neurologic evaluation. Red flag symptoms include waking up due to pain, worsening
pain on changing position, and continuous pain not relieved with over-the-counter headache medications.

Neurologic imaging with an MRI of the brain is
often the first step in diagnosis. Brain imaging showing contrast-enhancing masses can be suggestive of glioblastoma. Most cases can
be definitively diagnosed after surgery through histological testing. This takes place when a neuropathologist examines tissue or cells
under a microscope to help confirm a glioblastoma diagnosis.

Incidence and Mortality

In the United States, the average annual age-adjusted
incidence of glioblastoma is 3.2 per 100,000 population (or about 12,000 patients annually) with an average age of 64 at diagnosis. Glioblastoma
is 1.6 times more common in males compared with females and 2.0 times higher in Caucasians compared to African Americans, with lower
incidence in Asians and American Indians. Globally, glioblastoma incidence is highest in North America, Australia, and Northern and Western
Europe. Veterans who served in Iraq or Afghanistan are 26% more likely to develop glioblastoma, according to the U.S. Department of Veterans
Affairs and National Institutes of Health data, likely due to environmental exposures. Malignant primary brain tumors are the most frequent
cause of cancer death in children, are more common than Hodgkin lymphoma, ovarian and testicular cancer and are responsible for more
deaths than malignant melanoma.

Overall, the one-year relative survival rate
is about 40% for patients diagnosed in the United States. The five-year survival rate is only about 5%. Treatment outcome remains poor,
with a median survival rate of about 15 months.

Current Treatment/Management

A patient’s care team will take into account
age, functional status, medical history and medication tolerability when planning the best treatment. For most newly diagnosed patients,
the standard approach utilizes what is known as the Stupp protocol. Treatment is comprised of maximal surgical resection, which allows
for accurate histological diagnosis, tumor genotyping, and a reduction in tumor volume, followed by 6 weeks of radiotherapy and concomitant
daily temozolomide and a further 6 cycles of maintenance temozolomide. In patients with minimal functional impairment, the median overall
survival (“OS”) is 15 months for radiotherapy plus temozolomide versus 12 months for radiotherapy alone.

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Treatment options in the relapsed or recurrent
setting are less well defined, with no established standard of care and little evidence for any interventions that prolong OS. Indeed,
a significant proportion of patients may not even be eligible for second-line therapy. Options include further surgical resection, reirradiation,
systemic therapies such as carmustine or bevacizumab, combined approaches, or supportive care alone.

Patients may also be treated with tumor treatment
fields. This is a portable device placed on the scalp that uses mild electrical fields to try to interrupt cancer cell growth.

Standard-of-care treatments fail to specifically
eliminate tumor cells and are limited by incapacitating damage to surrounding normal brain and systemic tissues leading to lymphopenia
and many other detrimental side effects. All of this demonstrates that a more targeted immunotherapeutic approach is needed. Over the
last decade, emerging immunotherapies (such as monoclonal antibodies, oncolytic virus therapy, adoptive cell therapy, and cellular vaccines
therapy) aimed at improving specific immune response against tumor cells have brought a glimmer of hope to patients with GBM. Adoptive
cell therapy, including tumor-infiltrate lymphocytes (“TILs”) transfer and genetically engineered T cells transfer, is one
of the most significant breakthroughs in the field of immune-oncology. Chimeric antigen receptor (“CAR”) engineered autologous
T cells have produced sustained remissions in refractory lymphomas, but this approach needs further study in the treatment of solid tumors.
While there is significant potential with targeted immunotherapy in GBM, significant challenges remain, including primarily the difficulty
of crossing the BBB.

Bi-Specific Antibodies

The concept of bispecific antibodies was first
introduced in 1980s as a method to target multiple antigens by a single antibody. The recombinant bispecific antibodies are classified
into two types. The first are antibodies containing the crystallizable region (i.e., Fc-containing antibodies) and the second are antibody
derivatives without Fc regions. The Fc region is the tail region of an antibody that interacts with cell surface receptors called Fc
receptors and some proteins of the complement system. The mechanism of action of bispecific antibodies includes binding to the tumor
cells on one side through the Fab (antigen-binding region) portion of the antibody against the tumor-specific antigen (such as CD19,
HER2, EGFR, or GD2) and to the immune effector cells such as T cells and NK cells, which leads to activation of those immune effector
cells and Fc-receptor bearing phagocytic cells such as monocytes/macrophages that can also mediate direct lysis of the tumor cells.

Bispecific antibodies termed bispecific T cell
engagers (“BiTEs”) are monomeric proteins consisting of two antibody-derived single-chain variable fragments (“scFvs”)
translated in tandem. These constructs possess one effector-binding arm specific for the epsilon subunit of T-cell CD3 and an opposing
target-binding arm directed against an antigen that is expressed on the surface of tumor cells (e.g., EGFRvIII).

We believe EGFRvIII is an attractive target tumor specific antigen,
in part because it is specific to cancer cells and is not expressed in non-tumor tissue. Importantly, antibodies directed against EGFRvIII
are entirely tumor-specific and do not cross react with the wild-type receptor located on healthy cells. Therefore, by retargeting T
cells against the tumor-specific EGFRvIII antigen, we believe we can avoid killing healthy tissue and the related adverse effects. EGFRs
are involved in deregulated cancer signaling pathways, leading to atypical proliferation and growth of tumor cells. EGFRvIII is the most
common variant not presented in a major histocompatibility complex (“MHC”) -dependent manner and is seen in approximately
31 to 50% of patients with GBM and in a broad array of other cancers including breast and lung carcinoma. Lung and breast carcinoma are
the two main types of cancer that lead to secondary brain tumors (i.e., brain metastases) in about 25% of these patients. Among patients
with EGFRvIII-positive GBM, 37 to 86% of tumor cells express the mutated receptor, indicating that the mutation is translated with significant
consistency.

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Among patients with GBM, expression of EGFRvIII
is an independent, negative prognostic indicator. EGFRvIII also enhances the growth of neighboring EGFRvIII-negative tumor cells via
cytokine-mediated paracrine signaling and by transferring a functionally active oncogenic receptor to EGFRvIII-negative cells through
the release of lipid-raft related microvesicles. Recent research has also found that EGFRvIII is expressed in glioma stem cells, an important
consideration given the paradigm that tumor stem cells represent a subpopulation of cells that give rise to all differentiated tumor
cells. Altogether, the specificity, high frequency of surface expression and oncogenicity of the EGFRvIII mutation make it an ideal target
for antibody-based immunotherapy.

The divalent structure of BiTEs brings T cells
into close proximity to the tumor cell, creating a synapse. Following BiTE-mediated synapse formation, T cells proliferate, secrete pro-inflammatory
cytokines and express surface activation markers. Following BiTE-mediated synapse formation, T cells release perforin and granzyme proteases
that kill tumor cells. BiTEs are capable of mediating serial rounds of killing and can trigger specific tumor cell killing from naïve
T cells at exceedingly low concentrations and effector-to-target ratios.

It is well established that certain gliomas,
such as glioblastoma, are uniquely shielded from the immune system due to its location within the CNS. While this privilege is not absolute,
a significant proportion of tumors have been noted to be devoid of any TILs that can be redirected by bispecific T-cell engagers. In
those tumors that do demonstrate invasion by TILs, they are often induced to be dysfunctional and anergic by the suppressive tumor microenvironment.
Increased numbers of intratumoral CD8+ cytotoxic T lymphocytes (“CTLs”) have been associated with favorable outcomes in patients
with glioblastoma.

Concomitant administration of stimulated CTLs may therefore synergistically
enhance the efficacy of this treatment. The migration of T-cell engagers across the BBB may also be facilitated by activated T cells
which adhere to the brain microvascular endothelium and subsequently cross by diapedesis. Concurrent administration of activated functional
T cells could therefore enhance the trafficking of bispecific T-cell engagers and other therapeutics into the intracranial compartment,
increasing their density at the tumor site and thus the therapeutic effect.

Additionally, target cell killing with BiTE occurs
in the absence of regular MHC peptide antigen recognition and costimulation and is therefore resistant to certain immune escape mechanisms
affecting antigen presentation and those affecting generation of tumor-specific T cell clones. Because the CD3ε target of BiTE
antibody construct is the same in CD8+ and CD4+ T cells of any phenotype, they are all engaged, leading to a polyclonal T cell activation,
expansion and broad tumor cell killing.

Bispecific T-cell engagers offer immunotherapy
in a manufacturing format which is both scalable and standardizable. In contrast to CAR T cells, T-cell engagers do not require initial
lymphodepletion. Ex vivo manipulation of autologous cells has significant limitations, including the need for a centralized manufacturing
infrastructure with extensively trained laboratory personnel to genetically modify each patient’s own T cells, use viral transduction
which poses uncertain risks, are limited to the initial subset of T cells manipulated and infused, and still face uncertainty as to the
optimal T cell phenotype to infuse.

Our Product Pipeline

APTN-101

We have recently reported the development of
our first novel T cell engaging molecule, known as APTN-101, using our BRiTE technology. BRiTE focuses on the transport of difficult
to deliver T cell targeting agents across the BBB allowing access to the immunoprivileged brain and overcoming the challenges with other
immunotherapeutic approaches. This is accomplished by sequentially or simultaneously administering both BRiTE and specifically activated
T cells by adoptive transfer. APTN-101 was designed to specifically redirect T cells against tumors expressing a well-characterized,
mutated form of the EGFR, EGFRvIII, on a number of tumor types, including GBM. Because EGFRvIII is exclusively expressed on tumor cells,
but not normal healthy cells, it represents an ideal target for immunotherapy.

APTN-101 (EGFRvIII x CD3 BRiTE) successfully activates human T cells
against EGFRvIII expressing target cells, in the absence of any additional immunostimulatory signal, resulting in the secretion of Th-1-associated
cytokines and tumor-cell killing. APTN-101 is similarly effective in vivo. Intravenous administration of APTN-101 induced consistent
antitumor responses in mice bearing established, late-stage, aggressive, intracerebral patient-derived gliomas, rapidly achieving complete
remission rates as high as 75% in the absence of apparent toxicity. Given the exquisite tumor-specificity of APTN-101, it represents
a critical conceptual advance in safety contrary to target antigens having a promiscuous expression pattern.

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The concept of BRiTE is the combination of novel
T cell targeting agents with specifically activated polyclonal T cells. In order to exert antineoplastic affects against brain tumors,
both the T cell targeting agent and T cells need to efficiently access areas that have long been considered as immunoprivileged. While
circulating naïve T cells do not typically penetrate the CNS, activated T cells are known to cross the BBB to perform routine immunosurveillance
of the central nervous system (Figure 1).

Figure 1- The process of T cells crossing
the inflamed BBB is coordinating and sequential. Briefly, activated T cells initially arresting on the endothelium is mediated by the
lymphocyte-associated antigen-1 (“LFA- 1”) and α4β1-integrin expressed on the T cells, respectively binding to
the intracellular cell adhesion molecule 1 (“ICAM1”) and adhesion molecules vascular cell adhesion molecule 1 (“VCAM1”)
on brain endothelial cells. Subsequently, the T cell crawling and polarization exclusively involve LFA-1 and ICAM1/2 interactions. After
arriving at sites where are rich in the laminin isoform α4 but not laminin β5, the T cells use α6β1-integrin to
traverse the endothelial basement membrane.

Upon intravenous administration, the T cell targeting
agent (i.e., EGFRviii x CD3) binds to circulating T cells via its CD3 receptor and carries or “hitchhikes” the agent to tumors
located behind the BBB. Studies in aggressive orthotopic GBM models have revealed that adoptive transfer of activated T cells significantly
increases the biodistribution of intravenously administered EGFRvIII x CD3 BRiTE to orthotopic glioma (Figure 2).

Figure 2- Mass spectroscopy demonstrates that
pre-administration (four days) of ex vivo activated T cells increases the biodistribution of intravenously administered EGFRvIII x CD3
to the brain parenchyma.

BRiTE circumvents ordinary clonotypic T-cell
specificity, potentially allowing any T-cell, regardless of endogenous specificity or phenotype, to exert an anti-neoplastic effect.
In vivo experiments show that BRiTEs can reactivate potentially unresponsive, anergic T cells, such as those frequently encountered
among TIL populations thereby enhancing the spread of T cells reactive towards other antigens (epitope spreading). Proximal contact between
T cells and tumor cells could directly reactivate tumor infiltrating lymphocytes specific for cancer antigens other than directed by
BRiTE, without cross-presentation. The EGFRvIII x CD3 BRiTE molecule has the potential to directly activate and expand pre-existing T
cells among a polyclonal population that are specific for tumor antigens other than EGFRvIII. Indeed, others have discovered that by
re-activating pre-existing T cell clones using a CD3 binding bispecific antibody specific for Wilms’ tumor protein (WT1) it is
possible to induce effective and persistent epitope spreading responses to multiple antigens. If the clinical utility of this mechanism
of epitope spreading is confirmed, this could provide an exciting mechanism to combat tumor heterogeneity.

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Importantly, our data suggest that once APTN-101
reaches the brain, it can activate even suppressive regulatory T-cells (“Tregs”) to kill glioblastoma tumor cells by redirecting
their natural granzyme-mediated cytotoxic potential and enhance a cytotoxic immune response. These findings not only highlight a new
mechanism by which BRiTEs may circumvent certain aspects of Treg mediated suppression, but also have broader implications with regard
to the natural functional role of activated, tumor infiltrating Tregs that ordinarily suppress and kill cytotoxic T lymphocytes in the
tumor microenvironment.

By tethering cytotoxic effectors to target cells
without the need for antigen presentation via the MHC, BRiTEs can furthermore overcome tumor immune escape mechanisms, such as the downregulation
of MHC.

In addition to enhancing the biodistribution of EGFRvIII x CD3 BRiTE
to the brain, the activated polyclonal T cells (compared to the addition of no activated polyclonal T cells or naïve polyclonal
T cells) have the potential to restore effector T cells function at intracerebral sites (Figure 3) leading to cures in greater than 75%
of animals.

Figure 3- IV administration of activated T
cells enhances hEGFRvIII-CD3 bi-scFv efficacy against syngeneic, highly-invasive, orthotopic glioma (right panel) compared to IV administration
of naïve T cells when combined with hEGFRvIII-CD3 bi-scFv (left panel). The highly invasive murine glioma CT-2A-EGFRvIII was implanted
orthotopically in human CD3 transgenic mice (females, 8-10 weeks old, n=10 per group).

Next, we hypothesized that the increase in efficacy
observed with the pre-administration of activated polyclonal T cells would be abrogated if those T cells were to be blocked from entering
the CNS parenchyma. Natalizumab, a clinically approved drug for the treatment of multiple sclerosis, functions by binding to polyclonal
T cells and preventing their association with receptors involved in the process of extravasation. Remarkably, in cohorts of mice receiving
adoptive transfer of activated polyclonal T cells along with treatment with the extravasation blocking molecule natalizumab, efficacy
was decreased to levels observed in cohorts that did not receive adoptive transfer of activated polyclonal T cells (Figure 4).

Figure 4- Blocking T cell extravasation with
Natalizumab (αVLA-4) abrogates the observed increase in efficacy with adoptive cell transfer (n=8 per group). Natalizumab is a
clinically approved drug for the treatment of multiple sclerosis that functions by blocking T cell extravasation.

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We have also demonstrated an effective “antidote”
for any potential toxicity that may result from administration of the EGFRvIII x CD3 BRiTE in a clinical setting. By administering a
short peptide that spans the EGFRvIII mutation (PEPvIII), we have effectively blocked bispecific antibody function both in vitro
and in vivo, providing a tool highly likely to aid in safe clinical administration of any EGFRvIII targeted bispecific antibody.

The above data demonstrates that BRiTE technology
has the ability to transport difficult to deliver agents, including T cell targeting agents, across the BBB and demonstrate superior
antineoplastic activity in aggressive orthotopic models of GBM while having an acceptable safety profile. This newly uncovered hitchhiking
mechanism of drug delivery to the CNS provides an important tool to enhance the immunotherapy of brain tumors and has potentially far-reaching
consequences for the treatment of other CNS disorders, such as Alzheimer’s or Parkinson’s disease, where issues regarding
drug delivery to the CNS are relevant.

In summary, the results of preclinical studies
demonstrate that the EGFRvIII targeting BRiTE may provide a safe, highly effective therapeutic option for GBM patients. Future studies
will determine whether these results can be recapitulated in the clinical setting and whether BRiTEs favorably interact with other therapies
that are currently employed as a standard-of-care for GBM patients.

APTN-101 Clinical Studies

The proposed Phase 1 study will evaluate a novel
hEGFRvIII-CD3-biscFv Bispecific T cell engager (BRiTE) in patients diagnosed with pathologically documented supratentorial WHO grade
IV malignant glioma with an EGFR mutation (either newly diagnosed or at first progression/recurrence) at the Preston Robert Tisch Brain
Tumor Center at Duke University.

The primary objective of this Phase 1 study is
to determine the safety and tolerability of BRiTE and recommend Phase 2 dose of BRiTE injected with and without activated polyclonal
T-cells in among a patient population that includes newly diagnosed patients after completion of standard of care therapy consisting
of radiation and adjuvant temozolomide, and patients at first progression (defined as progression during or after standard of care radiation
and adjuvant temozolomide).

Another secondary objective is to describe the
pharmacokinetics (“PK”) in subjects treated with BRiTE. A population PK analysis will be performed to characterize the PK
of BRiTE using the software Nonlinear Mixed Effects Modeling (NONMEM, version 7.2). Different structural PK models (e.g., 1 and 2 compartment)
with linear or non-linear (e.g., Michaelis-Menten) kinetics will be fitted to the plasma concentration-time data of BRiTE.

Exploratory objectives include an evaluation
of the pharmacodynamics effect of BRiTE, an evaluation of the formation and incidence of anti-BRiTE antibodies, and a description of
overall survival and progression-free survival.

Our Intellectual Property

We strive to protect the proprietary technology
that we believe is important to our business, including our product candidates and our processes. We seek patent protection in the United
States and internationally for our product candidates, their methods of use and processes of manufacture, and any other technology to
which we have rights, as appropriate. Additionally, we have licensed the rights to intellectual property related to certain of our product
candidates, including patents and patent applications that cover the products or their methods of use or processes of manufacture. The
terms of the licenses are described below under the heading “License Agreement.” We also rely on trade secrets that may be
important to the development of our business.

We hold a world-wide exclusive license to three
issued or allowed United States patents and one pending Patent Cooperation Treaty (“PCT”) patent application covering the
enhanced delivery of drugs and other compounds to the brain and other tissues. The patents and patent applications that we licensed provide
patent terms or anticipated patent terms ranging from 2031 to 2039 without patent term extensions.

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Our success will in part depend on the ability
to obtain and maintain patent and other proprietary rights in commercially important technology, inventions and know-how related to our
business, the validity and enforceability of our patents, the continued confidentiality of our trade secrets, and our ability to operate
without infringing the valid and enforceable patents and proprietary rights of third parties. We also rely on continuing technological
innovation and in-licensing opportunities to develop and maintain our proprietary position.

We cannot be sure that patents will be granted
with respect to any of our pending patent applications or with respect to any patent applications we may own or license in the future,
nor can we be sure that any of our existing patents or any patents we may own or license in the future will be useful in protecting our
technology and products.

License Agreement

Patent License Agreement with Duke University

Effective January 11, 2023, we entered into a
patent license agreement (the “Duke License”) with Duke University, a nonprofit educational and research institution organized
under the laws of North Carolina (“Duke University”), whereby Duke University granted us an exclusive license with a right
to grant sublicenses to “BISPECIFIC EGFRvIII ANTIBODY ENGAGING MOLECULES,” “HUMAN BISPECIFIC EGFRvIII ANTIBODY AND
CD3 ENGAGING MOLECULES,” “CERTAIN IMPROVED HUMAN BISPECIFIC EGFRvIII ANTIBODY ENGAGING MOLECULES” and “ENHANCED
DELIVERY OF DRUGS AND OTHER COMPOUNDS TO THE BRAIN AND OTHER TISSUES” (together, the “precision medicine technology”).
With this technology, which we assumed pursuant to the Merger, we intend to develop our BRiTE Platform, a combination of an immune cell
engager with activated functional T-cells, which focuses on transporting difficult to deliver agents across the blood brain barrier,
allowing access to the immunoprivileged central nervous system. Under the Duke License, we are required to use commercially reasonable
efforts to obtain and retain the relevant governmental approvals and to commercialize the precision medicine technology. We must also
use reasonable efforts to reach certain commercialization and research and development milestones as outlined in the Duke License.

On August 8, 2024, we entered into a Sponsored Research Agreement
(the “2024 SRA”), which we assumed pursuant to the Merger, whereby Duke University agreed to perform research exploring the
administration methods of our BRiTE Platform for a fixed fee. The Duke License has been amended (the “First Amendment”) such
that we have the option to add any invention conceived as a result of the performance under the 2024 SRA to the license.

On February 18, 2025, we entered into an additional
Sponsored Research Agreement (the “2025 SRA”), whereby Duke University agreed to perform research to support the development
of GMP manufacturing procedures for the APTN-101 cell product to be infused with the hEGFRvIII-CD3 bi-scFv product as part of the BRiTE
study, and for the validation of those procedures in a GMP environment at Duke University’s Marcus Center for Cellular Cures.

As part of the consideration for the license,
we issued Duke University shares, representing 5% of our then issued and outstanding common stock on a fully diluted basis. Following
the Merger and additional issuances of common stock in 2025, Duke University holds approximately 1.2% of our shares of common stock on
a fully diluted basis. We also agreed to make payments based on clinical and commercial milestones, continuing royalty fees on any sales
made after approval by regulatory authorities and minimum annual royalty payments that began in 2025. These milestones include initiation
of a Phase II or Phase III clinical trials, submission of applications for market approval in multiple jurisdictions including the United
States, European Union and Japan and the initiation of post-approval commercial sales in the same jurisdictions. Based on an assumption
that all milestones related to the current development program are met during the course of the Duke License, these milestone payments
would total approximately $11.7 million. Under the terms of the Duke License, we must pay running royalties equal to low- to mid-single
digit percentages of annual net sales, depending on the level of sales by us, our sublicensees and affiliates in that year, and subject
to downward adjustment to low single digit percentages of our net annual sales in the event there is no valid claim of a patent for the
product, with minimum annual royalty levels established. We also must pay Duke University low to mid-double-digit percentages of any sublicensing
fees as set forth in the Duke License. We will be responsible for all patent expenses incurred by Duke University and have reimbursed
Duke University approximately $327,000 for patent expenses incurred, prior to the license, by Duke University for filing and prosecution
of the patent rights. Additionally, under the terms of the Duke License, we have reimbursed Duke University for patent expenses incurred
of approximately $55,000 and $31,000 for the years ended December 31, 2025 and 2024, respectively.

10

The term of the Duke License will extend until
the expiration of the last to expire patent rights, subject to early termination as set forth in the Duke License. The foregoing descriptions
of the Duke License, First Amendment and SRAs do not purport to be complete and are qualified in their entirety by the terms and conditions
of the Duke License, First Amendment and SRAs.

Manufacturing and Supply

We contract with third parties for the manufacturing
of all of our product candidates, and for pre-clinical and clinical studies and intend to continue to do so in the future. We do not
own or operate any manufacturing facilities and we have no plans to build any owned clinical or commercial-scale manufacturing capabilities.
We believe that the use of contract manufacturing organizations (“CMOs”) eliminates the need to directly invest in manufacturing
facilities, equipment and additional staff. Although we rely on contract manufacturers, our personnel and consultants have extensive
manufacturing experience overseeing CMOs.

We have produced the EGFRvIII x CD3 BRiTE in
a fashion suitable for clinical translational and compatible with clinical biologic manufacturing infrastructure. This has included generating
and certifying a Master Cell Bank and developing a scalable expression and tag-free purification and formulation process suitable for
clinical translation. On the basis of our data and development work, we have had a CMO produce clinical-grade EGFRvIII x CD3 BRiTE suitable
for clinical study.

As we further develop our product candidates,
we expect to consider secondary or back-up manufacturers for both active pharmaceutical ingredient and drug product manufacturing. To
date, our third-party manufacturers have met the manufacturing requirements for our product candidates in a timely manner. We expect
third-party manufacturers to be capable of providing sufficient quantities of our product candidates to meet anticipated full-scale commercial
demand but we have not assessed these capabilities beyond the supply of clinical materials to date. We currently engage CMOs on a “fee
for services” basis based on our current development plans. We plan to identify CMOs and enter into longer-term contracts or commitments
if and as we move our product candidates into Phase 3 clinical trials.

We believe alternate sources of manufacturing
will be available to satisfy our clinical and potential future commercial requirements; however, we cannot guarantee that identifying
and establishing alternative relationships with such sources will be successful, cost-effective, or completed on a timely basis without
significant delay in the development or commercialization of our product candidates. All of the vendors we use are required to conduct
their operations under current Good Manufacturing Practices (“cGMP”), a regulatory standard for the manufacture of pharmaceuticals.

Competition

The pharmaceutical industry is highly competitive
and characterized by intense and rapidly changing competition to develop new technologies and proprietary products, particularly in some
of the areas of high unmet medical need that we are targeting. Our potential competitors include both major and specialty pharmaceutical
and biotechnology companies worldwide, many of which have far greater resources and access to capital than we do. In particular, Context
Therapeutics, Vir Biotechnology and Janux Therapeutics, Inc. are studying immune cell engagers with different targets, and Amgen Inc.
and Genentech, Inc. (a wholly owned subsidiary of Roche Holding AG) have programs using a form of EGFRvIII x CD3 bispecific T cell engager
(although neither are using them in combination with activated T cells). Our success will be based in part on our ability to identify,
develop, and manage a portfolio of safe and effective product candidates that address the unmet needs of patients before our competitors.

Government Regulations

The FDA and other regulatory authorities at federal,
state and local levels, as well as in foreign countries, extensively regulate, among other things, the research, development, testing,
manufacture, quality control, import, export, safety, effectiveness, labeling, packaging, storage, distribution, record keeping, approval,
advertising, promotion, marketing, post-approval monitoring and post-approval reporting of drugs, such as those we are developing. Along
with our third-party contractors, we will be required to navigate the various preclinical, clinical, and commercial approval requirements
of the governing regulatory agencies of the countries in which we wish to conduct studies or seek approval or licensure of our product
candidates. The process of obtaining regulatory approvals and the subsequent compliance with appropriate federal, state, local, and foreign
statutes and regulations require the expenditure of substantial time and financial resources.

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FDA Regulation of Drugs

Before any of our drug product candidates may
be marketed in the United States, they must be approved by the FDA. The process required by the FDA before drug product candidates may
be marketed in the United States generally involves the following:

● completion of preclinical laboratory
tests and animal studies performed in accordance with the FDA’s current Good Laboratory Practices regulations;

● submission to the FDA of an
IND, which must become effective before human clinical trials may begin and must be updated annually or when significant changes are
made;

● approval by an independent
IRB or ethics committee for each clinical site before a clinical trial can begin;

● performance of adequate and
well-controlled human clinical trials to establish the safety and efficacy of the proposed product candidate for its intended purpose;

● preparation of and submission
to the FDA of a New Drug Application (“NDA”) after completion of all required clinical trials;

● a determination by the FDA
within 60 days of its receipt of an NDA to file the application for review;

● satisfactory completion of
an FDA Advisory Committee review, if required by the FDA;

● satisfactory completion of
an FDA pre-approval inspection of the manufacturing facility or facilities at which the proposed product is produced to assess compliance
with cGMP, and to assure that the facilities, methods, and controls are adequate to preserve the product’s continued safety, purity
and potency, and of selected clinical investigational sites to assess compliance with current Good Clinical Practices; and

● FDA review and approval of
the NDA to permit commercial marketing of the product for particular indications for use in the United States, which must be updated
annually and when significant changes are made.

The testing and approval processes require substantial
time, effort, and financial resources and each may take several years to complete. The FDA may not grant approval on a timely basis,
or at all, and we may encounter difficulties or unanticipated costs in our efforts to secure necessary governmental approvals, which
could delay or preclude us from marketing our product candidates. The FDA may delay or refuse approval of an NDA if applicable regulatory
criteria are not satisfied, or may require additional testing, information, and/or post-marketing testing and surveillance to monitor
safety or efficacy of a product candidate.

If regulatory approval of a product candidate
is granted, such approval may entail limitations on the indicated uses for which such product may be marketed. For example, the FDA may
approve the NDA with a Risk Evaluation and Mitigation Strategy (“REMS”) plan to mitigate risks, which could include medication
guides, physician communication plans, or elements to assure safe use, such as restricted distribution methods, patient registries, and
other risk minimization tools. The FDA also may condition approval on, among other things, changes to proposed labeling or the development
of adequate controls and specifications. Once approved, the FDA may withdraw the product approval if compliance with pre- and post-marketing
regulatory standards is not maintained or if problems occur after the product reaches the marketplace. The FDA may require one or more
post-market studies and surveillance to further assess and monitor the product’s safety and effectiveness after commercialization
and may limit further marketing of the product based on the results of these post-marketing studies. In addition, new government requirements,
including those resulting from new legislation, may be established, or the FDA’s policies may change, which could delay or prevent
regulatory approval of our product candidates under development.

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FDA Programs for Expedited Review and Increased
Exclusivity

A sponsor may seek approval of a product candidate
under Fast Track and Breakthrough Therapy programs designed to accelerate the FDA’s review and approval of new drug candidates
that meet certain criteria, and/or to receive increased exclusivity under the orphan drug program. We intend to pursue these programs
where our product candidates qualify.

Fast Track. A new drug candidate
is eligible for Fast Track designation if it is intended to treat a serious or life-threatening condition, fill an unmet medical need,
and demonstrate a significant improvement in the safety or effectiveness in the treatment of that condition.

A drug that receives Fast Track designation is
eligible for the following:

● more frequent meetings with
FDA to discuss the drug’s development plan and ensure collection of appropriate data needed to support drug approval;

● more frequent written correspondence
from FDA about the design of clinical trials;

● priority review to shorten
the FDA review process for a new drug from ten months to six months; and

● rolling review, which means
we can submit completed sections of its NDA for review by FDA, rather than waiting until every section of the application is completed
before the entire application can be reviewed.

Under the accelerated approval program, the FDA
may approve an NDA on the basis of either a surrogate endpoint that is reasonably likely to predict clinical benefit, or on a clinical
endpoint that can be measured earlier than irreversible morbidity or mortality, that is reasonably likely to predict an effect on irreversible
morbidity or mortality or other clinical benefit, taking into account the severity, rarity, or prevalence of the condition and the availability
or lack of alternative treatments. Fast Track designation and priority review do not change the standards for approval but may expedite
the development or approval process.

Breakthrough Therapy. A new drug
candidate is eligible for Breakthrough Therapy designation if it is intended to treat a serious condition and preliminary clinical evidence
indicates that the drug may demonstrate substantial improvement over available therapy on one or more clinically significant endpoints.

A drug that receives Breakthrough Therapy designation
is eligible for the following:

● All Fast Track designation
features;

● Intensive guidance from the
FDA on an efficient drug development program, beginning as early as Phase 1; and

● FDA organizational commitment
involving senior managers.

Orphan Drug Designation. Under
the Orphan Drug Act, the FDA may grant orphan drug designation to a drug candidate intended to treat a rare disease or condition, which
is generally a disease or condition that affects fewer than 200,000 individuals in the United States, or more than 200,000 individuals
in the United States and for which there is no reasonable expectation that costs of research and development of the drug for the indication
can be recovered by sales of the drug in the United States. Orphan drug designation must be requested before submitting an NDA. After
the FDA grants orphan drug designation, the generic identity of the therapeutic agent and its potential orphan use are disclosed publicly
by the FDA. Although there may be some increased communication opportunities, orphan drug designation does not convey any advantage in
or shorten the duration of the regulatory review and approval process.

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If a drug candidate that has orphan drug designation
subsequently receives the first FDA approval for the disease for which it has such designation, the product is entitled to orphan drug
exclusivity, which means that the FDA may not approve any other applications, including a full NDA, to market the same drug for the same
indication for seven years, except in very limited circumstances, such as if the second applicant demonstrates the clinical superiority
of its product or if the FDA finds that the holder of the orphan drug exclusivity has not shown that it can assure the availability of
sufficient quantities of the orphan drug to meet the needs of patients with the disease or condition for which the drug was designated.
Orphan drug exclusivity does not prevent the FDA from approving a different drug for the same disease or condition, or the same drug
for a different disease or condition. Among the other benefits of orphan drug designation are tax credits for certain research and a
waiver of the NDA application user fee.

As in the United States, designation as an orphan
drug for the treatment of a specific indication in the European Union must be made before the application for marketing authorization
is made. Orphan drugs in Europe enjoy economic and marketing benefits, including up to ten years of market exclusivity for the approved
indication unless another applicant can show that its product is safer, more effective or otherwise clinically superior to the orphan
designated product.

The inability to obtain or failure to maintain
adequate product exclusivity for our product candidates could have a material adverse effect on our business prospects, results of operations
and financial condition.

Other Healthcare Laws and Compliance Requirements

Our sales, promotion, medical education, clinical
research, and other activities following product approval will be subject to regulation by numerous regulatory and law enforcement authorities
in the United States in addition to the FDA, including potentially the Federal Trade Commission, the Department of Justice, the Centers
for Medicare and Medicaid Services (“CMS”), the U.S. Department of Health and Human Services (“DHHS”) Office
of Inspector General, and other divisions of DHHS, and state and local governments.

Our business and our relationships with customers,
physicians, and third-party payors are and will continue to be subject, directly and indirectly, to federal and state healthcare fraud
and abuse laws and regulations. These laws also apply to the physicians and third-party payors who will play a primary role in the recommendation
and prescription of our product candidates, if they become commercially available products. These laws may constrain the business or
financial arrangements and relationships through which we might market, sell and distribute our products and will impact, among other
things, any proposed sales, marketing and educational programs. There are also laws, regulations and requirements applicable to the award
and performance of federal grants and contracts. If our operations are found to be in violation of any of such laws or any other governmental
regulations that apply to them, we may be subject to penalties, including, without limitation, civil and criminal penalties, damages,
fines, disgorgement, the reimbursement of overpayments, the curtailment or restructuring of our operations, exclusion from participation
in federal and state healthcare programs, imprisonment, contractual damages, reputational harm, and diminished profits and earnings-any
of which could adversely affect our ability to operate our business and our financial results.

Restrictions under applicable federal and state
healthcare related laws and regulations include but are not limited to the following:

● the federal Anti-Kickback Statute;

● the civil federal False Claims
Act;

● the criminal federal False
Claims Act;

● the Health Insurance Portability
and Accountability Act, as amended by the Health Information Technology for Economic and Clinical Health Act of 2009, and its implementing
regulations (collectively, “HIPAA”);

● the civil monetary penalties
statute;

● federal transparency laws,
including the federal Physician Sunshine Act (“PSA”); and

● analogous or similar state,
federal, and foreign laws, regulations, and requirements.

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Efforts to ensure that our business arrangements
with third parties will comply with applicable healthcare laws and regulations involve substantial costs. Because of the breadth of these
laws and the narrowness of the statutory exceptions and safe harbors available, it is possible that governmental authorities will conclude
that our business practices do not comply with current or future statutes, regulations, or case law interpreting applicable fraud and
abuse or other healthcare laws and regulations. If our operations are found to be in violation of any of these laws or any other laws,
regulations, or other requirements that may apply to us, we may be subject to significant civil, criminal and administrative penalties,
damages, fines, imprisonment, restitution exclusion from government funded healthcare programs, corporate integrity agreements, deferred
prosecution agreements, debarment from government contracts and grants and refusal of future orders under existing contracts, contractual
damages, the curtailment or restructuring of our operations and other consequences. If any of the physicians or other healthcare providers
or entities with whom we expect to do business are found not to be in compliance with applicable laws, that person or entity may be subject
to criminal, civil, or administrative sanctions, including exclusions from government funded healthcare programs. Moreover, availability
of any federal grant funds which we may receive or for which we may apply is subject to federal appropriations law. Such grant funding
may also be withdrawn or denied due to a violation of the above laws and/or for other reasons.

Coverage and Reimbursement; Healthcare
Reform

Sales of pharmaceutical products depend significantly
on the extent to which coverage and adequate reimbursement are provided by third-party payers. Third-party payers include state and federal
government health care programs, managed care providers, private health insurers, and other organizations. Although we currently believe
that third-party payers will provide coverage and reimbursement for our product candidates, if approved, we cannot be certain of this.
Third-party payers are increasingly challenging the price, examining the cost-effectiveness and reducing reimbursement for medical products
and services. In addition, significant uncertainty exists as to the reimbursement status of newly approved healthcare products. The United
States government, state legislatures, and foreign governments have continued implementing healthcare reform and cost containment programs,
including price controls, restrictions on coverage and reimbursement and requirements for substitution of generic products. Adoption
of price controls and cost containment measures, and adoption of more restrictive policies in jurisdictions with existing controls and
measures, could further limit our net revenue and results. We might need to conduct expensive clinical studies to demonstrate the comparative
cost-effectiveness of our product candidates. Third-party payers might not consider the product candidates that we develop to be cost-effective
and not cover or sufficiently reimburse for their use. It is time-consuming and expensive for us to seek coverage and reimbursement from
third-party payers, as each payer will make its own determination as to whether to cover a product and at what level of reimbursement.
Thus, one payer’s decision to provide coverage and adequate reimbursement for a product does not assure that another payer will
provide coverage or that the reimbursement levels will be adequate. Moreover, a payer’s decision to provide coverage for a drug
product does not imply that an adequate reimbursement rate will be approved.

Foreign Regulation

In addition to regulations in the United States,
we will be subject to a variety of foreign regulations governing clinical trials and commercial sales and distribution of our product
candidates to the extent we choose to develop or sell any product candidates outside of the United States. The approval process varies
from country to country and the time may be longer or shorter than that required to obtain FDA approval. The requirements governing the
conduct of clinical trials, product licensing, pricing and reimbursement, and privacy, can vary greatly from country to country.

Employees

As of December 31, 2025, we had four employees,
all of whom are located in the United States. None of our employees is represented by a labor union or covered by a collective bargaining
agreement. We consider our relationship with our employees to be good.

Property

The Company owns no real property. We maintain
a month-to-month membership providing mail services and shared space for meetings and other business activities at 3540 Toringdon Way,
Suite 200, #250, Charlotte, North Carolina. The current rent is approximately $100 per month.

15

Litigation

From time to time, we may become involved in
various lawsuits and legal proceedings that arise in the ordinary course of business. However, litigation is subject to inherent uncertainties,
and an adverse result in these or other matters may arise from time to time that may harm business.

We are currently not aware of any pending legal
proceedings to which we are a party or of which any of our property is the subject, nor are we aware of any such proceedings that are
contemplated by any governmental authority.

Available Information

Our principal office is located at 3540 Toringdon
Way, Suite 200, #250, Charlotte, NC 28277 and our telephone number is (888) 609-1498. Our website is www.adaptinbio.com, and we
can be contacted at info@adaptinbio.com. We are subject to the informational requirements of the Exchange Act and file or furnish reports
and other information with the SEC. Such reports and other information filed by us with the SEC will be available free of charge on our
website at www.adaptinbio.com when such reports are available on the SEC’s website. The SEC maintains a website that contains
reports, information statements and other information that issuers file electronically with the SEC at www.sec.gov.

The contents of the websites referred to above are not incorporated
into this filing. Further, our references to the URLs for these websites are intended to be inactive textual references only.