UNCY US Equity☆

Item 1A. Risk Factors 24

Item 1B. Unresolved Staff Comments 51

Item 2. Properties 51

Item 3. Legal Proceedings 51

Item 4. Mine Safety Disclosures 51

Item 6. [Reserved] 52

Item 7A. Quantitative and Qualitative Disclosures about Market Risk 59

Item 8. Financial Statements and Supplementary Data F-1

Item 9A. Controls and Procedures 60

Item 9B. Other Information 61

Item 9C. Disclosure Regarding Foreign Jurisdictions that Prevent Inspections 61

Part III 62

Item 10. Directors, Executive Officers and Corporate Governance 62

Item 11. Executive Compensation 69

Item 14. Principal Accountant Fees and Services 75

Item 15. Exhibits and Financial Statement Schedules 76

Signatures 77

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CAUTIONARY

NOTE ON FORWARD-LOOKING STATEMENTS

This

Annual Report on Form 10-K contains forward-looking statements which are made pursuant to the safe harbor provisions of Section 27A of

the Securities Act of 1933, as amended (the “Securities Act”), and Section 21E of the Securities Exchange Act of 1934, as

amended (the “Exchange Act”). These statements may be identified by such forward-looking terminology as “may,”

“should,” “expects,” “intends,” “plans,” “anticipates,” “believes,”

“estimates,” “predicts,” “potential,” “continue” or the negative of these terms or other

comparable terminology. Our forward-looking statements are based on a series of expectations, assumptions, estimates and projections

about our company, are not guarantees of future results or performance and involve substantial risks and uncertainty. We may not actually

achieve the plans, intentions or expectations disclosed in these forward-looking statements. Actual results or events could differ materially

from the plans, intentions and expectations disclosed in these forward-looking statements. Our business and our forward-looking statements

involve substantial known and unknown risks and uncertainties, including the risks and uncertainties inherent in our statements regarding:

● our projected financial position and estimated cash burn rate;

● our estimates regarding expenses, future revenues and capital requirements;

● our ability to continue as a going concern;

● our need to raise substantial additional capital to fund our operation;

● the success, cost and timing of our clinical trials;

● our dependence on third parties in the conduct of our clinical trials;

● the results of market research conducted by us or others;

● our reliance on third-party suppliers and manufacturers;

● the success of competing therapies and products that are or become available;

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All

of our forward-looking statements are as of the date of this Annual Report on Form 10-K only. In each case, actual results may differ

materially from such forward-looking information. We can give no assurance that such expectations or forward-looking statements will

prove to be correct. An occurrence of, or any material adverse change in, one or more of the risk factors or risks and uncertainties

referred to in this Annual Report on Form 10-K or included in our other public disclosures or our other periodic reports or other documents

or filings filed with or furnished to the U.S. Securities and Exchange Commission (the “SEC”) could materially and adversely

affect our business, prospects, financial condition and results of operations. Except as required by law, we do not undertake or plan

to update or revise any such forward-looking statements to reflect actual results, changes in plans, assumptions, estimates or projections

or other circumstances affecting such forward-looking statements occurring after the date of this Annual Report on Form 10-K, even if

such results, changes or circumstances make it clear that any forward-looking information will not be realized. Any public statements

or disclosures by us following this Annual Report on Form 10-K that modify or impact any of the forward-looking statements contained

in this Annual Report on Form 10-K will be deemed to modify or supersede such statements in this Annual Report on Form 10-K.

This

Annual Report on Form 10-K may include market data and certain industry data and forecasts, which we may obtain from internal company

surveys, market research, consultant surveys, publicly available information, reports of governmental agencies and industry publications,

articles and surveys. Industry surveys, publications, consultant surveys and forecasts generally state that the information contained

therein has been obtained from sources believed to be reliable, but the accuracy and completeness of such information is not guaranteed.

While we believe that such studies and publications are reliable, we have not independently verified market and industry data from third-party

sources.

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RISK

FACTOR SUMMARY

Our

business is subject to numerous risks and uncertainties, including those highlighted in the section titled “Risk Factors,”

that represent challenges that we face in connection with the successful implementation of our strategy. The occurrence of one or more

of the events or circumstances described in the section titled “Risk Factors,” alone or in combination with other events

or circumstances, may have an adverse effect on our business, cash flows, financial condition and results of operations. Such risks include,

but are not limited to:

Risks

Relating to Our Financial Position and Capital Needs

Risks

Relating to the Development and Regulatory Approval of Our Product Candidates

-iv-

Risks

Relating to our Business and Operations

Risks

Relating to our Intellectual Property

General

Risk Factors

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PART

I

Throughout

this Annual Report on Form 10-K, references to “we,” “our,” “us,” the “Company,” “Unicycive,”

or “Unicycive Therapeutics” refer to Unicycive Therapeutics, Inc.

ITEM

1. BUSINESS

Overview

We are a biotechnology company dedicated to developing

treatments for certain medical conditions. Currently, two of our programs are focused on kidney disease that we believe have the potential

to offer medical benefit. As we grow the Company and build our team, we intend to focus on identifying medical conditions within and outside

of kidney disease. Our current development programs are focused on the development of two novel therapies: Renazorb, for treatment of

hyperphosphatemia in patients with chronic kidney disease, and UNI 494, for treatment of acute kidney injury (AKI). Renazorb and UNI 494

were initially developed by, and licensed to us from, Spectrum Pharmaceuticals (“Spectrum”) and Sphaera Pharmaceuticals, respectively.

Spectrum conducted a Phase 1 clinical trial with Renazorb in 2012 prior to the grant of our license in 2018. Sphaera conceived, and performed

initial characterization of, various potential pro-drug linkers, including the initial patent application, and performed some initial

physiochemical characterization and preliminary animal pharmacokinetic studies. As discussed herein, during 2020 and 2021 we have conducted

preclinical studies with UNI 494.

Chronic kidney disease (CKD) is the gradual loss

of kidney function that can get worse over time leading to lasting damage. Our initial focus is on developing drugs and getting them approved

in the US, and then to partner with global biopharmaceutical companies in the rest of the world. According to estimates by The Centers

for Disease Control and Prevention (CDC) in 2019, 37 million (approximately 15%) adults in the United States have CKD and, of these, approximately

2 million patients have CKD stage 3-5, and around 500 thousand patients with end-stage renal disease (ESRD) have hyperphosphatemia. In

the European Union (EU), around 20 million (approximately 8%) adults have CKD, more than 1 million CKD stage 3-5 patients, and approximately

180 thousand patients with ESRD have hyperphosphatemia. The number of patients with ESRD in the US is increasing steadily and is projected

to reach between 971,000 and 1,259,000 in 2030.

AKI is a sudden episode of kidney failure or kidney

damage (within the first 90 days of injury). After 90 days, the patient is considered to have progressed into CKD. AKI affects over 2

million U.S. patients and costs the healthcare system over $9 billion per year. AKI kills more than 300,000 patients per year in the U.S.

and is caused by multiple etiologies.

Our business model is to license technologies

and drugs, and pursue development, regulatory approval, and commercialization of those products in global markets. Many biotechnology

companies utilize similar strategies of in-licensing and then developing and commercializing drugs. We believe, however, that our management

team’s broad network, expertise in the biopharmaceutical industry, and successful track record gives us an advantage in identifying

and bringing these assets into our Company at an attractive price with limited upfront cost.

Pipeline

Our proprietary pipeline is comprised of our two product candidates

– Renazorb and UNI 494 – which are described below.

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UNI-218 (Renazorb)

Disease overview: hyperphosphatemia

Chronic kidney disease (CKD) is the gradual loss of kidney function

that can get worse over time leading to lasting damage. The stages of chronic kidney disease are shown below in table 1.

Table

1: adapted from The Renal Association (https://renal.org/information-resources/the-uk-eckd-guide/ckd-stages/)

eGFR = estimated glomerular filtration rate (a measure of kidney function)

Complications of CKD include electrolyte imbalances,

fluid build-up, anemia, bone disease, and heart disease. Hyperphosphatemia is an electrolyte disorder in which untreated elevated phosphate

levels in the blood lead to cardiovascular complications and vascular calcification. According to Kidney Disease Improving Global Outcome

(KDIGO) guidelines, hyperphosphatemia is defined as an abnormally high serum phosphate concentration >1.46 mmol/L. In healthy people,

phosphate levels are maintained as phosphate is absorbed from food and excreted in the urine and feces. In people with CKD, not enough

phosphate is excreted, leading to elevated levels of phosphate in the blood. In CKD, hyperphosphatemia is caused by a chronic dysregulation

of phosphates as a result of progressive kidney damage. According to a 2009 paper authored by Covic, hyperphosphatemia is associated with

increased risk of cardiovascular disease, metabolic bone disease, and all-cause mortality. According to a study completed by Palmer in

2011, it is estimated that all-cause mortality is increased by 18% for every 1 mg/dL increase in serum phosphate concentration. Hyperphosphatemia

is a major cause of morbidity in CKD patients, increasing the economic and clinical burden on patients and the health system.

According to Lederer in 2018, hyperphosphatemia occurs in at least

70% of patients with advanced (stage 5) CKD, which equates to approximately 500,000 patients. According to the 2019 National Chronic Kidney

Disease Fact Sheet (Centers for Disease Control and Prevention, 2019), it is estimated that 15% of US adults (i.e. approximately 37 million

people) have CKD. Furthermore, in a paper published by McCullough in 2019, the number of patients in the US with ESRD is increasing steadily

and is projected to reach between 971,000 and 1,259,000 in 2030.

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Current

treatment of hyperphosphatemia

The treatment goal for patients with hyperphosphatemia is focused on

controlling the level of phosphate in the body. Current Kidney Disease: Improving Global Outcomes, or KDIGO, guidelines recommend three

main strategies for managing hyperphosphatemia: diet restrictions, phosphate binders, and dialysis, as shown in figure 1 below.

Figure

1: KDIGO guidelines recommend 3 main strategies.

While KDIGO guidelines support the treatment of hyperphosphatemia with

phosphate binders in patients with CKD, they do not recommend one agent over another. Examples of different types of phosphate binders

are shown in figure 2 below.

Figure

2: Phosphate Binders

This means that physicians prescribe their medication of choice, usually

based on clinical and patient factors. In CKD patients on dialysis, hyperphosphatemia is most commonly treated with non-calcium phosphate

binders.

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The

Unmet Medical Need for Treatment of Hyperphosphatemia

The mechanism of action and what we believe to be the advantages and

disadvantages of various phosphate binders are shown below.

Table

2: Adapted from Covic and Rastogi, 2013.

In 2005, Unruh, ML published a paper that showed

poor adherence to treatment is common in patients with ESRD and has been associated with an increased risk of mortality. In addition,

poor adherence to phosphate binder therapy has been associated with failure to adequately control serum phosphorus concentrations as shown

in a publication by Arenas, MD and others in 2010. Results from a study of 233 patients on maintenance dialysis from three different dialysis

units in the US showed that patients took a mean of 11 ± 4 medications with a median daily pill intake of 19 as shown by Chiu,

YW in 2009. Phosphate binders accounted for 49 ± 19% of the total pill burden, with a median pill count of 9. Only 38% of patients

in this study were adherent to their prescribed phosphate binder therapy and adherence decreased significantly with increased pill count

also shown by Chiu, YW in 2009 publication.

Potential strategies to improve adherence to phosphate

binders in patients with ESRD include: (i) a reduction in pill size and number, (ii) improvement of palatability, and (iii) a reduction

in associated adverse effects as published in a study by Covic and Rastogi in 2013.

Therefore, we believe there is a current need

for better phosphate binders that have high and rapid phosphate binding, alongside a reduced pill burden for better medication compliance.

Background on Renazorb

Renazorb (lanthanum dioxycarbonate) is a second-generation

phosphate binding agent utilizing proprietary nanoparticle technology for the treatment of hyperphosphatemia in CKD patients. In September

2012 a Phase 1 single-center clinical trial was completed in the United States with Renazorb studying 32 healthy volunteers. Four sequential

dose cohorts of 8 subjects each (6 active and 2 placebo) received Renazorb at 1500, 3000, 4500, or 6000 mg/day, taken orally in 3 divided

doses within 15 min after meals, for five consecutive days. The primary endpoint of the study was the evaluation of safety, and the secondary

endpoint was the phosphate binding capacity of Renazorb as judged by the level of phosphorus in feces and urine. We believe the study

indicated that Renazorb was minimally absorbed to the systemic circulation and was well-tolerated at doses up to 6000 mg/day. Renazorb

significantly reduced urine phosphate excretion and significantly increased fecal phosphate excretion at doses at and above 3000 mg/day.

The mean overall change in phosphorus from baseline in both urine and feces, across all treatment groups, showed a dose-response trend

that was statistically significant (p<0.0001 and p=0.0004, respectively). The mean reduction in urine phosphorus excretion was not

significant at 1500 mg/day (p=0.3676), but was significant at doses of 3000 (p=0.0004), 4500 (p<0.0001), and 6000 (p=0.0001) mg/day.

The mean increase in fecal phosphorus excretion was significant at doses of 1500 (p=0.0358), 3000 (p=0.0006), 4500 (p=0.0026), and 6000

(p<0.0001) mg/day. The doses resulted in no serious adverse events (SAEs) and all patients completed the study.

Renazorb Purchase Agreement

On September 20, 2018, we entered into an Assignment and Asset Purchase

Agreement (the “Renazorb Purchase Agreement”) with Spectrum Pharmaceuticals, Inc. (“Spectrum”), pursuant to which

we purchased certain assets from Spectrum, including Spectrum’s right, title, interest in and intellectual property related to Renazorb

RZB 012, also known as RENALANTM (“Renalan”) and RZB 014, also known as SPI 014 (“SPI” and together with

Renalan, the “Compounds”). Pursuant to the Renazorb Purchase Agreement, in consideration for the Compounds, we issued 313,663

shares of common stock to Spectrum.

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Additionally,

the Renazorb Purchase Agreement provides that until the earlier of (i) 36 months from the first date on which our stock trades on a public

market, or (ii) the date upon which we attain a public market capitalization of $50,000,000 or greater, we are required to issue additional

shares of our common stock as may be needed to ensure Spectrum maintains a 4% ownership of our issued and outstanding common stock on

a fully-diluted basis. Fully-diluted shares of common stock for purposes of the Renazorb Purchase Agreement assumes conversion of any

security convertible into or exchangeable or exercisable for common stock or any combination thereof, including any common stock reserved

for issuance under a stock option plan, restricted stock plan, or other equity incentive plan approved by the Board of Directors of the

Company immediately following the issuance of additional shares of our common stock (but prior to the issuance of any additional shares

of common stock to Spectrum). We are also required to pay Spectrum 40% of all of our sublicense income for any sublicense granted to

certain sublicensees during the first 12 months after the Closing Date (as that term is defined in the Renazorb Purchase Agreement) and

20% of all other sublicense income. Our payment obligations to Spectrum will expire on the twentieth (20th) anniversary of

the Closing Date of the Renazorb Purchase Agreement.

Mechanism of Action

Renazorb binds to phosphates and forms an insoluble

lanthanum phosphate complex which is then excreted via the feces. This results in reduction of serum phosphate levels.

In rat studies, Renazorb exhibited comparable binding kinetics compared

to lanthanum carbonate (Fosrenol). This was evident from comparable reduction in the phosphate level in urine of rats following administration

of equivalent doses of lanthanum through Renazorb (i.e. LDC or lanthanum dioxycarbonate) vs lanthanum dioxycarbonate tetrahydrate (i.e,

LCTH or Fosrenol) (see Fig 3).

Figure

3: Urine phosphate levels in rats following comparable lanthanum dosing through Renazorb (LDC) or Fosrenol (LCTH)

Animal studies to evaluate the potential efficacy of Renazorb versus

sevelamer hydrochloride (Renagel) in rats and dogs demonstrated significant lowering of phosphate levels in both urine and serum. In animal

toxicology studies no unexpected toxicity was found and systemic absorption was extremely low that is consistent with Fosrenol.

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The chemical design of Renazorb allows for smaller

tablet size and fewer pills versus currently available phosphate binder alternatives, specifically with a dosing regimen of only one

tablet per meal. The tablet is designed to disintegrate in the stomach after swallowing and disperse the product in a short period of

time at a pH ≥3.0.

Clinical Trial Experience

In September 2012 a Phase 1 single-center clinical trial was completed

in the United States with Renazorb studying 32 healthy volunteers. Four sequential dose cohorts of 8 subjects each (6 actives and 2 placeboes)

received Renazorb at 1500, 3000, 4500, or 6000 mg/day, taken orally in 3 divided doses within 15 min after meals, for five consecutive

days. The primary endpoint of the study was the evaluation of safety, and the secondary endpoint was the phosphate binding capacity of

Renazorb as judged by the level of phosphorus in feces and urine. We believe the study indicated that Renazorb was minimally absorbed

to the systemic circulation and was well-tolerated at doses up to 6000 mg/day. Renazorb significantly reduced urine phosphate excretion

and significantly increased fecal phosphate excretion at doses at and above 3000 mg/day. The mean overall change in phosphorus from

baseline in both urine and feces, across all treatment groups, showed a dose-response trend that was statistically significant (p<0.0001

and p=0.0004, respectively). The mean reduction in urine phosphorus excretion was not significant at 1500 mg/day (p=0.3676), but was significant

at 3000 (p=0.0004), 4500 (p<0.0001), and 6000 (p=0.0001) mg/day, as shown in the figure below.

The mean increase in fecal phosphorus excretion

was significant at 1500 (p=0.0358), 3000 (p=0.0006), 4500 (p=0.0026), and 6000 (p<0.0001) mg/day. The doses resulted in no serious

adverse events (SAEs) and all patients completed the study.

Potential advantages of Renazorb

Renazorb is a phosphate binder for the treatment of hyperphosphatemia

in patients with CKD and is intended to be administered as a tablet that will be swallowed whole at mealtimes. CKD patients typically

have co-morbidities, which often require them to be on strict pill schedules. Current phosphate binder products such as Fosrenol, Renagel/Renvela

and Phoslo involve patients needing to take multiple and/or larger pills (on average, 9 pills/day), in addition to other, non-phosphate

binder pills they sometimes need to take, resulting in poor adherence to the prescribed drug therapy (Figure 4 below). Lower molecular

weight and no water of hydration with Renazorb as compared with Fosrenol allows Renazorb to be dosed in smaller mass. In this regard,

we believe that the combined effect of smaller pill size, lower number of pills, and improved palatability with Renazorb versus currently

available phosphate binders is likely to lead to improved patient compliance and more effective disease management.

Figure

4: Size comparisons of different phosphate binders

Market Potential

The worldwide market for hyperphosphatemia agents

is estimated at ~$2.5 billion growing at a 5.3% CAGR (Fortune Business Insights, Hyperphosphatemia Treatment Market, 2021-2028).

According to a study conducted by Syneos Health for the Company, based on the market data, the total US market makes up over $1 billion

of the that total.

Based on the available data on overall efficacy, safety and compliance,

we believe that Renazorb is well-positioned to become a product of choice in the multi-billion phosphate binder market.

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Manufacturing

We do not own or operate manufacturing facilities

for the production of clinical or commercial quantities of our product candidates. We currently have no plans to build our own clinical

or commercial scale manufacturing capabilities. If and when any of our product candidates are approved, we plan to obtain manufacturing

capacity through contract manufacturing organizations (CMOs) to meet projected needs for commercial sale quantities and serve patient

needs.

With regards to manufacturing, testing and potential

commercial supply of Renazorb, we have entered into an agreement with Shilpa Medicare Ltd based in India. According to the terms of the

agreement Unicycive will pay the vendor $2 million in the first calendar year when the net revenue reaches $10 million from sales of Renazorb

following its approval by the FDA and commercial supply of the product by the vendor (First Payment). Thereafter, we will pay $2 million

per year for four consecutive years, after the first year’s payment, for the total payments of $10 million, provided all commercial

supplies are continued to be manufactured and supplied by the vendor. Unicycive is not obligated to make any payments to the vendor until

FDA approval of the product is obtained and commercial revenue is generated.

Regulatory Strategy for Renazorb

Feedback from the FDA

We received additional guidance on the regulatory

pathway for Renazorb from the U.S. Food and Drug Administration (FDA) following a Type C meeting in March 2022, in which the Agency confirmed

that a single clinical bioequivalence study in healthy volunteers, together with the previously agreed-upon 6-month mouse toxicology study

can support the New Drug Application (NDA) filing of Renazorb through a 505(b)(2) pathway.

We reached an agreement with the Agency on the

clinical study design including the dose of Renazorb and Fosrenol, sample size and the primary endpoints of the bioequivalence study.

The Agency confirmed that no additional clinical studies would be required for the NDA application.

BE Study Description

Based on guidance from the FDA, we are initiating a randomized, open

label, two-way crossover BE study to establish pharmacodynamic bioequivalence between Renazorb and Fosrenol. The study will enroll 32

individuals per treatment sequence for a total of 64 evaluable subjects. An adequate number of subjects will be screened and randomized

in order to get 64 evaluable subjects into the study. The primary endpoint of the study is LS mean change in urinary phosphate excretion

from baseline to the evaluation period. The study will consist of a screening period, 2 dosing periods, a washout period, and a follow-up

period. The study design is presented in the diagram below:

We believe that our continued collaborative interactions with the FDA

will serve us well to be able to file our NDA. Activities in support of each of the requirements recommended by FDA are underway. We intend

to hold additional discussions with FDA during the second half of 2022 to confirm their concurrence with our dataset and NDA submission

strategy with the goal to file NDA by the end of 2022 or early 2023.

UNI

494

Disease

overview: acute kidney injury (AKI)

Acute kidney injury (AKI) — a loose collection

of syndromes characterized by a sudden decrease in estimated glomerular filtration rate (eGFR) — is estimated to affect 2–3

people per 1,000 individuals in the United States as shown in a study published in The Journal of the American Medical Association (JAMA)

by Kellum, JA in 2012. AKI is a serious condition characterized by a sudden decline in kidney function that can lead to kidney

failure. AKI, and CKD can form a continuum (see figure below) whereby initial kidney injury can lead to persistent renal injury, eventually

leading to CKD as shown in a 2017 study published by Chawla, LS in Nature Reviews Nephrology.

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AKI

is defined as an abrupt decrease in kidney function occurring over 7 days or less, whereas CKD is defined by the persistence of kidney

disease for a period of >90 days. AKD describes acute or subacute damage and/or loss of kidney function for a duration of between

7 and 90 days after exposure to an AKI initiating event (Figure 6).

Figure

6: Adapted from Nature Review-Nephrology; Chawla LS et al. 2017

In the United States, approximately 1% of patients

admitted to hospitals have AKI at the time of admission. The estimated incidence rate of AKI during hospitalization is 2-5%. AKI develops

within 30 days postoperatively in approximately 1% of general surgery cases as shown in a paper by Kheterpal S in Journal Anesthesiology

and arises in up to 67% of intensive care unit (ICU) patients as published in a paper by Goldberg R, 2008 in Advances in Chronic

Kidney Disease. In recipients of solitary kidney transplants, 21% developed AKI within the first 6 months after transplantation as shown

in a paper published by Panek R in 2016 in Clinical Transplantation.

In a prospective national cohort study that used

an electronic AKI alert, the incidence of AKI was 577 per 100,000 population. Community-acquired AKI accounted for 49.3% of all incidence

episodes, and 42% occurred in the context of pre-existing chronic kidney disease. The 90-day mortality rate was 25.6%, and 23.7% of episodes

progressed to a higher AKI stage as published by Holmes J et al. in Clinical Journal of American Society of Nephrology in 2016.

The KDIGO criteria for AKI are shown below in Table 3. According to

a study by Susantitaphong et al in 2013, using the KDIGO definition, an estimated 1 in 5 adults and 1 in 3 children worldwide experience

AKI during a hospital episode of care.

Table

3: KDIGO criteria for AKI

The incidence of AKI varies among different patient

populations and is shown below in Table 4. A 2018 study by Pavkov reported that the total number of hospitalizations with AKI increased

from 953,926 in 2000 to 1,823,054 in 2006 and to 3,959,560 in 2014. Among persons with diabetes, AKI hospitalizations increased by 139%,

from 23.1 to 55.3 per 1,000 persons and by 230% among persons without diabetes, from 3.5 to 11.7 per 1,000 persons (both p<0.001).

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Hospital-acquired

AKI is linked to 3 main areas: sepsis, procedures, and drug toxicity as shown below in Table 4.

Table

4: Adapted from Hoste et al. 2018

Current

treatment of acute kidney injury

Treatment options for AKI include continuous renal replacement therapy,

renal transplant, and dialysis. In a majority of cases the damage to the kidney is irreversible, and the patient needs to have a renal

transplant or be on dialysis for life. There are no approved medicines to treat AKI; there is therefore a high unmet medical need. If

approved, UNI 494 (a patented pro-drug of nicorandil) has the potential to be a first-in-class drug for the treatment of AKI.

Background

on nicorandil

Nicorandil,

marketed in such products as Ikorel and Dancor, is indicated for the treatment of chronic stable angina pectoris. It is not currently

approved in the United States but has been approved for use in Australia, the United Kingdom and most of Europe, and in India, Japan,

South Korea, and Taiwan. Nicorandil is a dual-action potassium channel opener that relaxes vascular smooth muscle through membrane hyperpolarization

via increased transmembrane potassium conductance and increased intracellular concentration of cyclic guanosine monophosphate (GMP).

It is shown to dilate normal and stenotic coronary arteries and reduces both ventricular preload and afterload.

Nicorandil

in acute kidney injury

The

kidney has one of the highest mitochondrial densities in the body. Both acute and chronic kidney disease is associated with mitochondrial

loss and impaired replacement, which subsequently results in increased oxidative damage and cellular injury. The diagram below in Figure

7 (Che R, 2014) shows how mitochondrial dysfunction can lead to kidney disease.

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Figure 7:

Che R, 2014: Mitochondria Dysfunction

Since mitochondrial dysfunction is an important factor in the pathogenesis

of AKI, the mitochondria have emerged as a therapeutic target for treatment as published in a study by Ishimoto Y in 2016 in Journal Nephrology

Dialysis Transplantation. In preclinical studies, nicorandil has been shown to improve mitochondrial function by blocking the opening

of mitochondrial permeability transition pores (MPTP) and by stabilizing mitochondria against oxidative stress as published by Afzal,

M in 2016 in Journal of Cardiovascular Pharmacology.

Figure

8 below shows the potential mechanisms of how nicorandil can improve mitochondrial function in renal disease.

Nicorandil

has been reported to have a potential protective effect in the kidneys in nonclinical (Shiraishi 2014, Tamura 2012, Tanabe 2012) and

human studies (Zhan 2018, Ma 2018). Further, no significant differences in pharmacokinetic parameters of nicorandil have been observed

in patients with normal renal function as compared to those with impaired renal function (Molinaro 1992).

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In animal studies, nicorandil has demonstrated efficacy in multiple

standard models of kidney disease (see Table 5). Notably, these effects occur in a blood pressure-independent manner, indicating that

these beneficial effects are not simply a result of decreasing pressure-mediated kidney damage, but a direct beneficial effect on the

kidney:

Table

5: Efficacy of nicorandil in standard models of kidney disease

Limitations

of Nicorandil

Despite

these promising results, development of nicorandil for use in acute kidney injury has not been successfully pursued to date. Nicorandil

possesses at least two features that may limit its use in this clinical setting. First, nicorandil has a short half-life in humans of

approximately 1 hour, which results in the need to dose nicorandil multiple times per day to achieve sustained blood levels.

Second,

nicorandil is well tolerated by most patients, with less than 10% of patients reporting side-effects after 30 days of treatment, and

roughly 70% remaining on nicorandil at one year. Similar to nitrates, headache is the most common side effect to nicorandil, occurring

in roughly one third of patients. Other relatively common side effects are: dizziness, flushing, malaise and gastro-intestinal upset.

However, nicorandil has been associated with rare but serious ulcerations in the gastrointestinal tract. The chance of this rare but

potentially severe side effect increases with higher doses and long term use of this drug, and heals after drug withdrawal. A recent

population-based study of this drug’s association with GI ulceration or perforation has been reported. This study, based on more

than 600,000 randomly selected patients, found a 43% increase in the risk of GI ulceration and a 60% increase in the risk of GI perforation.

This effect appears dose-dependent and limits the maximum labeled dose of nicorandil in Europe.

UNI

494: a Pro-drug of Nicorandil

UNI

494 is a patented pro-drug that was designed to be absorbed into the systemic circulation, and once absorbed, to release nicorandil into

the bloodstream. By avoiding direct exposure to the gastrointestinal tract of nicorandil, it is believed that UNI 494 may be able to

minimize or avoid the gastrointestinal side effects of nicorandil. Also, based on the rate of conversion of UNI 494 to nicorandil in

the systemic circulation, UNI 494 may offer greater and/or more prolonged exposure to nicorandil for the treatment of patients with acute

kidney injury. Our technology for UNI 494 is licensed from Sphaera Pharmaceutical Private Limited, a Singapore-based company (“Sphaera”),

with offices in India and the US. We have the global, exclusive license to UNI 494. Sphaera conceived of and performed initial characterization

of various potential pro-drug linkers, including the initial patent application, and performed some initial physiochemical characterization

and preliminary animal pharmacokinetic studies.

In

October 2020, we completed preclinical studies in rats and dogs demonstrating systemic exposure to nicorandil following oral dosing of

UNI 494. In dogs, oral dosing of UNI 494 produced up to 4 times greater systemic exposure to nicorandil compared with literature data

on equimolar doses of nicorandil itself.

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We

have selected rat and dog as the most suitable species for the GLP toxicology program for UNI 494, which we plan to commence in 2022.

Sphaera

License Agreement

On

October 1, 2017, we entered into an exclusive license agreement (the “Sphaera License Agreement”) with Sphaera Pharma Pte.

Ltd., a Singaporean pharmaceutical corporation (“Sphaera”). Pursuant to the Sphaera License Agreement, we acquired an exclusive

royalty-bearing worldwide license to develop, make, have made, use, practice, research, distribute, lease, sell, offer for sale, license,

import or otherwise dispose of certain rights owned or controlled by Sphaera and/or any of its affiliates, related to UNI 494 (the “UNI

494 Rights”). We also acquired a non-exclusive license to certain know-how and technology related to the UNI 494 Rights. Sphaera

conceived of and performed initial characterization of various potential pro-drug linkers, including the initial patent application,

and performed some initial physicochemical characterization and preliminary animal pharmacokinetic studies.

Under

the terms of the Sphaera License Agreement, we are obligated to pay to Sphaera, on a quarterly basis, a running royalty of 2% of our

net sales (including our affiliates) in connection with the sales of UNI 494; provided, however, that if we are required to make royalty

payments to one or more third parties whose patent rights would be infringed by the exercise of the UNI 494 Rights, we may reduce such

running royalty due to Sphaera by the amount of such third-party royalty rate.

We

are also required to pay to Sphaera certain milestone payments, including, upon our initiation of a second clinical trial; $50,000 at

the time the first patient in such trial is dosed; an additional $50,000 within 30 days of completion of such trial; and at the time

the FDA accepts a New Drug Application for UNI494, $1.65 million. In addition, we are responsible for the prosecution of patent rights,

and any related costs and expenses for patent prosecution and maintenance.

We

also have the right, but not the obligation, to defend the UNI 494 rights during the term of the Sphaera License Agreement; provided,

however, that if we determine not to prosecute or maintain such rights in any country, we must provide ninety (90) days written notice

to Sphaera. We may terminate the Sphaera License Agreement at any time by providing thirty (30) days’ written notice to Sphaera.

Additionally, in the event that either we or Sphaera breach any of our respective material obligations, the non-breaching party may,

in its sole discretion, have the right to terminate the Sphaera License Agreement, provided that it give the breaching party written

notice specifying the nature of the breach and amounts of running royalty payments due, if any. In such an occurrence, the termination

notice is effective ninety (90) days from receipt of the notice if the breaching party has failed to cure the breach.

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Clinical

trials for UNI 494 in AKI

UNI

494 is currently in preclinical development. We plan to conduct repeat-dose animal toxicology studies and other IND-enabling preclinical

studies in 2022 prior to initiating clinical development of UNI 494 in AKI.

It

is challenging to conduct clinical trials in AKI trials due to the multiple etiologies of AKI. We believe that UNI 494 should be evaluated

in clinical trials focusing on a few select etiologies in which UNI 494 has a very strong mechanistic rationale based on nicorandil clinical

experience in terms of protection of kidney function and secondary benefits.

Based on our understanding of mechanism of action of the drug, we are

in discussions with key opinion leaders (KOLs) to identify t the AKI subsets where UNI 494 can be most active and subsets of AKI patients

who are most likely to benefit from UNI-494. We are planning to conduct preclinical studies in animal models to further explore the efficacy

and development path in the AKI indication. We have also identified patient populations where we would not likely evaluate UNI 494 in

clinical trials, including patients with prior history of gastrointestinal ulcerations. This will become exclusion criteria in future

clinical trials for UNI 494.

Regulatory

Strategy for UNI 494

Nicorandil is already approved in Europe and Asia

for the treatment of heart disease. We believe there is a possibility these historical Nicorandil data, along with preclinical and clinical

data with UNI 494 itself, can be utilized for streamlined US FDA review of UNI 494. While pre-clinical requirements to start a clinical

program for an IND would be similar for UNI-494 as for NCE (New Chemical Entity). We believe that the vast clinical data set from Nicorandil

will potentially help us to expedite the clinical development program with the FDA.

Market

Potential

According

to a 2017 article by Silver and Chertow, the current cost of care for AKI in the U.S. is estimated to be between $5.4 to $24 billion

per year. In England, inpatient costs related to AKI are estimated to make up 1% of the total National Health Service budget. With no

effective treatment for AKI, it is not possible to definitively state a market figure. However, with the high cost and burden of AKI,

we believe a conservative market estimate is approximately $3 billion in the US alone. The lack of effective therapeutic interventions

for AKI means that UNI 494 has the potential to be the first drug approved for the treatment of AKI. AKI is a heterogeneous disease.

We plan to target a more homogeneous AKI population for UNI 494 by focusing on kidney injury caused by complications from heart failure,

surgeries, drugs, and contrast induced nephropathy.

Competition

We

operate in a highly competitive and regulated industry that is subject to rapid and frequent changes. We face significant competition

from organizations that are pursuing products that would compete with the product candidates we are developing and the same or similar

products that target the same conditions we intend to treat. Due to our limited resources, we may not be able to compete successfully

against these organizations, which include many large, well-financed and experienced pharmaceutical and biotechnology companies, as

well as academic and research institutions and government agencies.

Intellectual

Property

Our

commercial success depends in part on our ability to obtain and maintain proprietary protection for our product candidates, as well as

novel discoveries, product development technologies, and know-how.

Our

commercial success also depends in part on our ability to operate without infringing on the proprietary rights of others and to prevent

others from infringing our proprietary rights. Our policy is to develop and maintain protection of our proprietary position by, among

other methods, filing or in-licensing U.S. and foreign patents and applications related to our technology, inventions, and improvements

that are important to the development and implementation of our business.

We

also rely on trademarks, trade secrets, know-how, continuing technological innovation, confidentiality agreements, and invention assignment

agreements to develop and maintain our proprietary position. The confidentiality agreements are designed to protect our proprietary information

and the invention assignment agreements are designed to grant us ownership of technologies that are developed for us by our employees,

consultants, or other third parties. We seek to preserve the integrity and confidentiality of our data and trade secrets by maintaining

physical security of our premises and physical and electronic security of our information technology systems. While we have confidence

in our agreements and security measures, either may be breached, and we may not have adequate remedies. In addition, our trade secrets

may otherwise become known or independently discovered by competitors.

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With

respect to both licensed and company-owned intellectual property, 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 filed by us in the future, nor can we be sure that any

of our existing patents or any patents that may be granted to us in the future will be commercially useful in protecting our commercial

products and methods of using and manufacturing the same.

Renazorb

Patent Portfolio

Our

Renazorb patent portfolio includes one family of granted United States patents, with related applications pending, and an additional

family of granted foreign patents, with related applications also pending. Granted and pending claims offer various forms of protection

for Renazorb including claims to compositions of matter, pharmaceutical compositions, specific forms (such as polymorphs of lanthanum

dioxycarbonate), methods of making the composition of matter, and methods for treating elevated levels of phosphate in the blood using

Renazorb. These United States patents and applications, and their foreign equivalents, are described in more detail below.

Both

the U.S. patent family and the foreign patent family containing claims to Renazorb and related compounds were filed in 2011. Exclusive

of patent term extension, the U.S. patents from this family containing claims covering Renazorb has a statutory expiration date in 2031.

Corresponding patents granted in Canada, Europe (validated in multiple European Patent Convention member states), Japan, China, Australia,

and other countries have statutory expiration dates in 2031.

In

some cases, granted United States patents claiming Renazorb have a longer statutory term than the corresponding foreign patents. This

results from the USPTO’s practice of granting patent term adjustments for prosecution delays originating at the USPTO. Such adjustments

are generally not available under foreign patent laws. If Renazorb is approved for marketing in the United States, under the Hatch-Waxman

Act we may be eligible for up to five years patent term extension for a granted United States patent containing claims covering Renazorb.

Similar term extensions may be available in Europe, Japan, Australia, and certain other foreign jurisdictions. The amount of any such

term extension, and the identity of the patent to which it would apply, are dependent upon several factors including the duration of

the development program and the date of marketing approval.

The

most relevant granted United States patents with claims covering Renazob are listed below, along with their projected expiration dates

exclusive of any patent term extension.

Patent Number Title Projected Expiration

UNI

494

We

believe that we have a strong global intellectual property position, substantial know-how and trade secrets relating to UNI 494. As of

October 28, 2020, we have one granted U.S. patent that is exclusively licensed to us from Sphaera Pharma Pte Ltd. In addition, we have

one application that we own. The granted U.S. patent is directed to methods of making UNI 494, and it is expected to expire in 2032.

The PCT application is directed to methods of using UNI 494, and to other compositions of matter and their uses. Should U.S. and other

global patents issue from this PCT application, they are expected to expire in 2040.

-14-

Government

Regulations

Government

authorities in the United States at the federal, state and local level, including the FDA, the FTC and the DEA, extensively regulate,

among other things, the research, development, testing, manufacturing, quality control, approval, labeling, packaging, storage, recordkeeping,

promotion, advertising, distribution, marketing and export and import of products such as those we plan to develop and market. For both

the products under development and to be marketed, failure to comply with applicable regulatory requirements can, among other things,

result in suspension of regulatory approval and possible civil and criminal sanctions. Regulations, enforcement positions, statutes and

legal interpretations applicable to the pharmaceutical industry are constantly evolving and are not always clear. Significant changes

in regulations, enforcement positions, statutes and legal interpretations could have a material adverse effect on our financial condition

and results of our operations.

Additionally,

future healthcare legislation or other legislative proposals at the federal and state levels could bring about major changes in the affected

health care systems, including statutory restrictions on the means that can be employed by brand and generic pharmaceutical companies

to settle Paragraph IV patent litigations. We cannot predict the outcome of such initiatives, but such initiatives, if passed, could

result in significant costs to us in terms of costs of compliance and penalties associated with failure to comply.

Pharmaceutical

Regulation in the United States

In

the United States, the FDA regulates drugs under the FDCA and its implementing regulations. 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. Failure to comply with the applicable U.S. requirements at any time during the product development

process, approval process or after approval may subject an applicant to administrative or judicial sanctions. These sanctions could include

the FDA’s refusal to approve pending applications, withdrawal of an approval, a clinical hold, Warning Letters, product recalls,

product seizures, total or partial suspension of production or distribution of product(s), injunctions, fines, refusals of government

contracts, restitution, disgorgement or civil or criminal penalties. Any agency or judicial enforcement action could have a material

adverse effect on us.

FDA

approval is required before any new unapproved drug or dosage form, including a new use of a previously approved drug or a generic version

of a previously approved drug, can be marketed in the United States.

The

process required by the FDA before a new drug may be marketed in the United States generally involves:

● Approval by an IRB at each clinical site before each trial may be initiated;

● Submission to the FDA of an NDA;

● FDA review and approval of the NDA.

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Preclinical

Studies

When

developing a branded product and bringing it to market, the first step in proceeding to clinical studies is preclinical testing. Preclinical

tests are intended to provide a laboratory or animal study evaluation of the product to determine its chemistry, formulation and stability.

Toxicology studies are also performed to assess the potential safety of the product. The conduct of the preclinical tests must comply

with federal regulations and requirements, including GLPs. The results of these studies are submitted to the FDA as part of an IND application

along with other information, including product chemistry, manufacturing and controls and a proposed clinical trial protocol. Long-term

preclinical tests, such as animal tests of reproductive toxicity and carcinogenicity, may continue concurrently with the IND application.

Clinical

Trials

Clinical

trials involve the administration of the investigational new drug to human subjects under the supervision of qualified investigators

in accordance with GCP requirements, which include the requirement that all research subjects provide their informed consent in writing

for their participation in any clinical trial. Clinical trials are conducted under protocols detailing, among other things, the objectives

of the trial, the parameters to be used in monitoring safety, and the effectiveness criteria to be evaluated. A protocol for each clinical

trial and any subsequent protocol amendments must be submitted to the FDA as part of the IND. In addition, an IRB at each institution

participating in the clinical trial must review and approve the plan for any clinical trial before it is initiated at that institution.

Information about certain clinical trials must be submitted within specific timeframes to the NIH for public dissemination on their www.clinicaltrials.gov

website.

Human

clinical trials are typically conducted in three sequential phases, which may be distinct, or overlap or be combined:

Progress

reports detailing the results of the clinical trials must be submitted at least annually to the FDA and more frequently if serious adverse

events occur. Phase 1, Phase 2, and Phase 3 trials may not be completed successfully within any specified period, or at all. Furthermore,

the FDA or the sponsor may suspend or terminate a clinical trial at any time on various grounds, including a finding that the research

subjects are being exposed to an unacceptable health risk. Similarly, an IRB can suspend or terminate approval of a clinical trial at

its institution if it is not being conducted in accordance with the IRB’s requirements or if the drug has been associated with