Company: BDRX
Filing Date: 2025-05-01
Form Type: DRS
Source: 0001214659-25-006756
Chunk: 32

Company: Biodexa Pharmaceuticals Plc
Filing Date: 2025-05-01
Form: DRS
Chunk 32
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 is raised through the sale of equity or convertible
debt securities, the issuance of these securities could result in further dilution to our stockholders.

In addition, subsequent to
December 31, 2024 through the date of this registration statement, we have sold and issued (i) 17,398,000,000 Ordinary Shares, pursuant
to the ELOC, to the Investor resulting in gross proceeds of $4.9 million, and (ii) 1,533,490,000 Ordinary Shares in satisfaction of a
commitment fee in connection with the ELOC.

Except as otherwise noted,
all information in this prospectus reflects and assumes (i) no exercise of any warrants issued in this offering and (ii) no
exercise of the underwriters’ option to purchase additional Depositary Shares and/or Series L Warrants, or any combination thereof.

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<div align='center'>BUSINESS</div>

Company Overview

We are a clinical stage biopharmaceutical company developing a pipeline of innovative products for the treatment of diseases with unmet medical needs, including familial adenomatous polyposis, or FAP, non-muscle invasive bladder cancer, or NMIBC, type 1 diabetes, or T1D, and rare/orphan cancers of the brain.

In April 2024 we licensed eRapa, a proprietary formulation of rapamycin, from Rapamycin Holdings, Inc. d/b/a Emtora Biosciences, Inc., or Emtora. Rapamycin is an mTOR inhibitor. As a central regulator of cell metabolism, growth, proliferation and survival, the mTOR pathway is activated during various cellular processes including tumor formation and angiogenesis. Through the use of nanotechnology and pH sensitive polymers, eRapa is designed to address the poor bioavailability, variable pharmacokinetics and toxicity generally associated with the currently available forms of rapamycin. An ongoing Phase 2 study of eRapa in NMIBC is scheduled to report results in mid-2025.

Tolimidone is a selective activator of the enzyme lyn kinase which increases phosphorylation of insulin substrate -1, thereby amplifying the signaling cascade initiated by the binding of insulin to its receptor. Lyn kinase modulates key intracellular functions such as proliferation, differentiation, apoptosis, migration and metabolism. In fat cells, lyn kinase increases utilization of insulin, thus decreasing blood sugar without having an effect on insulin production. In pancreatic islets, activation of lyn kinase promotes beta cell survival and