Forward looking statements This presentation has been prepared by Aerpio Pharmaceuticals ("we", "us" or, the "Company") and includes forward-looking statements. All statements contained in this presentation other than st

Corporate Presentation January 7, 2019

Forward looking statements This

presentation has been prepared by Aerpio Pharmaceuticals ("we", "us" or, the "Company") and includes forward-looking statements. All statements contained in this presentation other than statements of historical

facts, including statements regarding our product candidates, their therapeutic potential and development plans, our future results of operations and our financial position, our business strategy and plans and our objectives for future operations,

are forward-looking statements. Forward-looking statements speak only as of the date hereof unless it is stated otherwise. Although we believe that the expectations reflected in these forward-looking statements are reasonable, these statements

relate to our strategy, our intellectual property position, future operations, future financial position, future revenue, projected costs, prospects, plans, objectives of management and expected market growth, and involve known and unknown risks,

uncertainties and other factors that may cause our actual results, levels of activity, performance or achievements to be materially different from any future results, levels of activity, performance or achievements expressed or implied by these

forward-looking statements including those contained in our public filings with the Securities and Exchange Commission. This presentation also contains estimates and other statistical data made by independent parties and by us. Management bases all

estimates and projections as to events that may occur in the future (including projections of revenue, development plans and timing of clinical trial results) upon their best judgment as of the date of this presentation. Whether or not such

estimates or projections may be achieved will depend upon the Company achieving its overall business objectives and the availability of funds. The Company does not guarantee that any of these projections will be attained. Actual results will vary

from the projections, and such variations may be material. New risks emerge from time to time, and except as required by law, neither we nor any other person makes any representation as to the accuracy or completeness of such data or undertakes any

obligation to update such data after the date of this presentation. You should, therefore, not rely on these forward-looking statements as representing our views as of any date subsequent to the date of this presentation. This presentation may

contain trade names, trademarks or service marks of other companies. The Company does not intend the use or display of other parties' trade names, trademarks or service marks to imply a relationship with, or endorsement or sponsorship of,

these other parties. Solely for convenience, the trade names, trademarks or service marks in this presentation are referred to without the symbols and , but such references should not be construed as any indicator that their respective

owners will not assert, to the fullest extent under applicable law, their rights thereto.

Overview of Aerpio Diabetes leads to

vascular leaks over time due to glucose insult. These leaks have three significant effects: Diabetic macular edema (DME) driven by fluid leaking behind retina Damage to kidneys leading over time to kidney dialysis (median survival <5 years)

Diabetic neuropathy and amputations Erectile dysfunction Aerpio has developed AKB-9778, which is a Tie2 activator, which seals vascular leaks improving health Delay or reduce DME (saving $35,000/year) Might delay or reduce kidney dialysis (saving

$50,000/year) Might reduce multiple hospitalizations per year for other issues Aerpio is currently running a trial in diabetic retinopathy (DR) to demonstrate the ability to seal the leaky vasculature DR would represent a biomarker and the best

moment to treat these patients to delay or prevent damage to the eye, kidney and other effects

Overview of Aerpio The diabetic market

is very large in the US 30 million diabetics 8.4 million estimated to have DR 1.6 million diagnosed with DR Following only patients diagnosed with DR and assuming a price of $10,000 per patient, the US market may be $16 billion. Adding in Europe,

Japan, Canada takes the market to over $30 billion Aerpio has a very strong patent portfolio in TIE-2 activation Phase 2b data expected in March 2019

Aerpio's IBD Drug Aerpio has

entered into a partnership for its IBD drug with Gossamer (Faheem Hasnain & Sheila Gujrathi) for $20 million upfront, $400 million of milestones and mid-teens royalties as well as a percentage of the proceeds if the asset is ever sold $8 billion

potential market HIF drug with good safety profile distinguishing it from other IBD drugs like Humira and steroids Strong efficacy data in mice Phase 1b human trial completed by end of this year Daily pill rather than an injection

Tie2 Biology & the Critical Role of

Diabetic complications are a result of

progressive blood vessel damage due to chronic diabetes The Problem Vascular leak and pathology leads to devastating consequences in diabetes The Solution Potential to reverse vascular leak by activating Tie2 with AKB-9778 The Opportunity ~380

million diabetics world-wide increasing to 590 million by 2035 ~132 million with retinopathy today Estimated 7 million Americans with NPDR Estimated 4-5 million Americans with NPDR and nephropathy

Tie2 is a transmembrane receptor found

on endothelial cells, the foundation for vascular stability Tie2 activity Maintains integrity of endothelial cell junctions Enhances endothelial cell function and viability Inhibits vascular inflammation Inactive Tie2 = Vascular

Destabilization Promotes pathologic vascular leak and neovascularization Active Tie2 is essential for vascular stability Tie2 Receptor Phosphate

Blood Vessel Cross Section Tie2

Receptor Activated by Ang-1 X X VE-PTP Inactivates Tie2 by dephosphorylation X X AKB-9778 Inhibits VE-PTP = Restoring blood vessel stability Inhibiting VE-PTP with AKB-9778 reactivates Tie2 and restores endothelial cell stability even with Ang-2

present Ang-1 = Ang-2 = AKB-9778 = P P P P P P Ang-1 - Angiopoietin 1 Ang-2 - Angiopoietin 2 VE-PTP - Vascular endothelial protein tyrosine phosphatase

Diabetic Retinopathy and AKB-9778

TIME-2 Clinical Data

Diabetic retinopathy progresses over

time and can lead to blindness if untreated Diabetic eye disease is a progressive disease characterized by worsening vascular damage Vascular damage in the eye leads to leakage of fluid and proteins in the surrounding retinal tissue Eventually the

damage may be severe enough to cause significant vision loss and potentially blindness NPDR - Non-proliferative diabetic retinopathy PDR - Proliferative diabetic retinopathy DME - Diabetic macular edema Retinal Photographs

Progression of Diabetic Retinopathy

TIME-2 Design & Analyses DRSS

- Diabetic Retinopathy Severity Score bid - twice daily * 3 patients withdrew from trial before efficacy measurements determined Study Eye Fellow Eye Primary Analysis Secondary Analysis (Prospective) Patients with DME Three Arms (n =

144*) SQ/Systemic+Study Eye bid SQ AKB-9778+ monthly x 3 IVT Sham (n=46) bid SQ AKB-9778+ monthly x 3 IVT Lucentis(n=48) bid SQ Placebo+ monthly x 3 IVT Lucentis (n=47) Primary Endpoint Change in retinal thickness at month 3 Secondary Measurements

2-step DRSS change at month 3 Patients with DRSS 2-6 in study and fellow eye Two Arms (n = 128) SQ/Systemic+ Fellow Eye bid SQ AKB-9778+None(n=90) bid SQ Placebo+None(n=38) Patients with DRSS of 1 in fellow eye removed (unable to measure 2-step

improvement in DRSS) Prospective Measurements 2-step DRSS change at month 3 SQ SQ

TIME-2: Change in retinal thickness

over time p = 0.008 p = 0.02 Campochiaro P, et al. Ophthalmology, Aug. 2016; Vol. 123. Phase 1 data showed efficacy as monotherapy in DME prompting testing of monotherapy in phase 2a No efficacy seen as monotherapy in primarily VEGF-driven disease

(DME) Vascular stabilizing effect of combination therapy significantly greater than either agent alone -110

Risk of vision-threatening events

(DME, hemorrhage, retinal detachment, etc.) increases with each step Treatment of DR is generally not initiated until later in disease due to the drawbacks of currently available interventions (e.g. laser, intraocular injection) Early intervention

could slow or prevent disease progression Progression of diabetic eye disease is measured using a discrete 11-step scale (Diabetic Retinopathy Severity Score - DRSS) DME - Diabetic macular edema DR - Diabetic retinopathy NPDR -

Non-proliferative diabetic retinopathy PDR - Proliferative diabetic retinopathy Klein R et al., Arch Ophthalmol., 2001, Vol. 119. The FDA bar: 2-step improvement at 12 months AKB-9778 has already achieved 2-step improvement at 3 months

in TIME-2 trial Aerpio target market

Percentage of Patients with a

2-Step Improvement in DRSS @ 3 Months Study eye assessment of diabetic retinopathy improvement from TIME-2 study DRSS - Diabetic retinopathy severity score Campochiaro P, et al. Ophthalmology, Aug. 2016; Vol. 123.

Percentage of Patients with a

2-Step Improvement in DRSS @ 3 Months Fellow eye assessment of diabetic retinopathy improvement from TIME-2 study DRSS - Diabetic retinopathy severity score Campochiaro P, et al. Ophthalmology, Aug. 2016; Vol. 123. 2-step improvement

expected to increase at one-year timepoint (on-going TIME-2b study) Placebo rate of improvement consistent with sham control in Lucentis RISE/RIDE studies (3% at M3, M6 and 12) Consistent and bilateral 2-step improvement in DRSS from TIME-2 support

biologic activity of AKB-9778

RISE/RIDE: Improvement of DRSS over

time DRSS - Diabetic retinopathy severity score Ophthalmology. 2012 Apr;119(4):789-801; Ranibizumab for diabetic macular edema: results from 2 phase III randomized trials: RISE and RIDE Diabetic retinopathy does not improve on its own Active

therapy improves DRSS over time

Validation by Roche and Regeneron:

Aerpio's approach to treating DR via Tie2 activation supported by anti Ang 2 results Roche/Genentech BOULEVARD study (RG7716) Dugel, P. RG7716 in Diabetic Macular Edema: Results from the Phase 2 BOULEVARD Study. Angiogenesis,

Exudation, and Degeneration; February 10, 2018; Miami, FL. Brown, D. Nesvacumab in Diabetic Macular Edema: Results from the Phase 2 RUBY Study. Angiogenesis, Exudation, and Degeneration; February 10, 2018; Miami, FL. Regeneron RUBY study

Promising rationale for development

in DR AKB-9778 Monotherapy ability to control DR in equivalent manner to Lucentis (approved therapy for the treatment in DR) Consistent effects seen bilaterally, study and fellow eye Placebo performed in accordance with contemporaneous DR studies:

no improvement in absence of therapeutic intervention Regulatory path precedent set by Lucentis ( 2-step improvement @ 1-year) AKB-9778 product attributes support a potential market-leading profile for patients with DR, good vision, and no

center involved DME No need for intraocular injections and no increase in frequency of visits to ophthalmologist Treats both eyes via systemic delivery (>70% patients with DR have bilateral disease) Potential to prevent progression to vision

threatening events of PDR and DME May improve diabetes-induced nephropathy and compromise of other vascular beds AKB-9778 development: DR vs. DME

Diabetic Retinopathy: Patient

Numbers and Market Estimates

NPDR is highly underdiagnosed and a

very large market Geography Estimated Prevalence Diabetes (1)* Estimated Prevalence of DR (2)* Estimated Prevalence of NPDR (2,3)* U.S. 24 8.4 6.7 Europe 50 17 14 China 98 34 27 Japan 12 4 3 ROW 196 69 55 TOTAL 380 132 106 * Patients Millions

1. Guariguata, L., et al. Diabetes Res and Clin Practice, 2014; 103: 137-14 2. Yau J, et al. Diabetes Care. 2012;35:556-564. (10.2337/dc11-1909) 3. NPDR = all DR minus PDR Potential AKB-9778 NPDR opportunity 100 million Sev PDR Moderate PDR

Mild PDR Very Severe NPDR Severe NPDR Moderate NPDR Mild NPDR

AKB-9778: TIME-2 Study -

Kidney Function Analysis

1 2 4 3 Progression of diabetic eye

and kidney disease suggest a common pathologic process

TIME-2 UACR data: Baseline

proteinuria subgroup ( 30 mg/g) SC - Subcutaneous UACR - Urine albumin/creatinine ratio p = 0.03, unadjusted (All SC AKB-9778 vs. SC placebo) p = 0.006, adjusted for baseline UACR, HgbA1c, and systolic blood pressure (All SC

AKB-9778 vs SC placebo)

AKB-9778: TIME-2b Study

TIME-2b: Clinical trial design Phase

2b study in pts with moderate to severe non-proliferative diabetic retinopathy (NPDR) without DME 1o Endpoint: 2-step improvement in DRSS at 48 weeks Key 2o Endpoints: development of DME/PDR, DR progression, renal function Enrollment

commenced June 2017, enrollment closed February 2018 at 167 patients, data expected March 2019 DME - Diabetic macular edema DR - Diabetic retinopathy DRSS - Diabetic retinopathy severity score PDR - Proliferative diabetic

AKB-9778: Primary Open-Angle

AKB-9778 Monotherapy AKB-9778 +

Lucentis Lucentis monotherapy SE FE SE FE SE FE Mean Baseline IOP (mmHG) 15.8 15.4 15.9 16.1 15.2 15.8 Mean from BL (mmHG) -1.4 -1.4 -1.0 -1.5 0.1 -0.1 t-test BL-Mo 3 (p-value) <0.01 <0.01 <0.05 <0.01 0.88 0.84

BL = baseline; SE = study eye; FE = Fellow eye Statistically significant reductions in intraocular pressure were observed in non-glaucoma patients in the TIME-2 study Reduction of IOP increased to 2-2.5 mm Hg in patients with baseline IOPs

16 mm Hg, similar to prostaglandin analogs in normotensive glaucoma Dirks et al. Adv Ther. 23:3, 2006 Khawaja et al. Ophthalmology 121:1501, 2014 Stenkula and Wettrell, Graefe's Arch Clin Exp Ophthalomol 218:96, 1982

Larger IOP changes seen in patients

with higher baseline pressure Baseline IOP 16 mmHg Baseline IOP < 16 mmHg Mo 1 Mo 2 Mo 3 Mo 1 Mo 2 Mo 3 Change in IOP (mmHg) 4 2 0 -2 -4 * * * * * * * p<.01

Loss of Tie2 function leads to

increased IOP and glaucoma phenotype in mice and humans

Ocular hypertension and pathology of

glaucoma: AKB-9778 presents a potentially new MOA that affects the main pathway in IOP reduction Aqueous flows out through the trabecular meshwork (TM) and Schlemm's canal Aqueous flows into the anterior chamber from the ciliary body Eye