NeOnc Technologies (Nasdaq: NTHI) details Phase 1 NEO212 results and Phase 2 plans
Rhea-AI Filing Summary
NeOnc Technologies Holdings, Inc. furnished an update on its oral brain cancer drug candidate NEO212, sharing full Phase 1 dose-escalation results and outlining next development steps. The Phase 1/2 trial reached Maximum Tolerated Dose at 810 mg in Cohort 5, and the Recommended Phase 2 Dose was set at 610 mg (Cohort 4), with 400 mg as the starting dose for the Phase 2a metastasis cohort.
Although Phase 1 was primarily a safety study, NeOnc reported early signs of anti-tumor activity, including durable disease control in heavily pretreated glioblastoma and brain metastasis patients. Across cohorts, the company highlighted low levels of systemic NEO212 metabolites and reported no clinically meaningful myelosuppression, hepatic, or renal toxicity, which are common concerns with standard temozolomide therapy.
NeOnc plans to move NEO212 into Phase 2 expansion cohorts focused on recurrent central nervous system cancers and intends to request a Type B (End-of-Phase 1) FDA meeting to discuss safety, pharmacology, preliminary efficacy, Phase 2 design, and a potential accelerated approval pathway.
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Insights
NeOnc advances NEO212 with a defined Phase 2 dose, encouraging safety and early activity.
The company now has a clear clinical foundation for NEO212, having defined a Maximum Tolerated Dose at 810 mg and a Recommended Phase 2 Dose at 610 mg. Reporting no clinically meaningful myelosuppression or hepatic/renal toxicity addresses key limitations of standard temozolomide in brain cancers.
Early efficacy signals in recurrent glioblastoma and brain metastasis patients, including durable disease control in heavily pretreated cases, provide preliminary support for the drug’s mechanism targeting MGMT-mediated resistance. These data remain early and from a small Phase 1 cohort, so future outcomes will depend on larger, controlled Phase 2 trials.
NeOnc’s plan to seek a Type B End-of-Phase 1 FDA meeting and design randomized Phase 2 studies in recurrent GBM and brain metastases aligns with an accelerated approval strategy. Subsequent regulatory feedback and Phase 2 results will be central to understanding NEO212’s potential role versus current standards of care.
UNITED STATES
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| Item 7.01. | Regulation FD Disclosure. |
On March 4, 2026, NeOnc Technologies Holdings, Inc. (the “Company”) issued a press release announcing data from the dose-escalation portion of its Phase 1/2 clinical trial for NEO212 (the “Data”). A copy of the press release is furnished as Exhibit 99.1 to this Current Report on Form 8-K.
On March 4, 2026, the Company hosted an investor conference call to discuss the Data. Furnished as Exhibit 99.2 and Exhibit 99.3 hereto are the investor presentation that the Company used in connection with its presentation at the investor conference call and a transcript of the investor conference call, respectively.
The information in this Item 7.01, Exhibit 99.1, Exhibit 99.2 and Exhibit 99.3 furnished hereto shall not be deemed “filed” for purposes of Section 18 of the Securities Exchange Act of 1934, as amended (the “Exchange Act”), or otherwise subject to the liabilities of that section, nor shall it be deemed incorporated by reference in any filing under the Securities Act of 1933, as amended, or the Exchange Act, except as expressly set forth by specific reference in such a filing.
| Item 9.01. | Financial Statements and Exhibits. |
| (d) | Exhibits |
| Exhibit No. | Description | |
| 99.1 | Press Release, dated March 4, 2026 | |
| 99.2 | Investor Presentation | |
| 99.3 | Transcript | |
| 104 | Cover Page Interactive Data File (embedded within the Inline XBRL document) |
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SIGNATURES
Pursuant to the requirements of the Securities Exchange Act of 1934, the registrant has duly caused this report to be signed on its behalf by the undersigned hereunto duly authorized.
| Dated: March 6, 2026 | NeOnc Technologies Holdings, Inc. | ||
| By: | /s/ Amir Heshmatpour | ||
| Name: | Amir Heshmatpour | ||
| Title: | Chief Executive Officer, President and Executive Chairman | ||
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Exhibit 99.1
NeOnc Technologies Reports Phase 1 Dose-Escalation Results for Dosing and Toxicity and Determination of Recommended Phase 2 Dose for Oral NEO212; Management to Host KOL Conference Call Today at 9 a.m. ET
CALABASAS, Calif., March 4, 2026 (GLOBE NEWSWIRE) -- NeOnc Technologies Holdings, Inc. (Nasdaq: NTHI) (“NeOnc” or the “Company”), a multi-Phase 2 clinical-stage biopharmaceutical company developing novel therapies for central nervous system (CNS) cancers, today announced data from the dose-escalation portion of its Phase 1/2 clinical trial for NEO212, the Company’s novel oral bio-conjugated therapy and will host a conference call to discuss the data today at 9:00am ET.
NeOnc has formally notified the FDA that the Phase 1 dose-escalation portion of the NEO212-01 Phase 1/2 clinical trial has reached Maximum Tolerated Dose (MTD) at Cohort 5 (810 mg, Days 1–5, 28-day cycle) following a second Dose-Limiting Toxicity. In accordance with protocol-defined stopping rules, dose escalation has been halted, no further patients will be enrolled at 810 mg, and the Recommended Phase 2 Dose (RP2D) has been set at 610 mg (Cohort 4). For the Phase 2a metastasis cohort, the starting dose will be 400 mg (Cohort 3).
Notably, although Phase 1 was mainly designed to assess safety, tolerability, and identify the MTD, promising signs of clinical efficacy appeared during this phase of the study. These efficacy signs—including indications of lasting disease control in heavily pretreated patients with recurrent GBM and brain metastases—were observed within the dose-escalation groups.
The emergence of measurable anti-tumor activity in Phase 1 offers early clinical confirmation of NEO212’s therapeutic potential and supports the Company’s progress into the Phase 2 segment of the trial.
“These early efficacy signals, observed even within a dose-escalation safety study, provide meaningful clinical validation of NEO212’s therapeutic potential,” said Amir Heshmatpour, Chairman and CEO of NTHI. “With RP2D now established, we believe NeOnc is entering Phase 2 with positive clinical momentum and a clear development pathway.”
The transition into Phase 2 will focus on further assessing efficacy at the RP2D in specific expansion cohorts, aiming to generate strong clinical data to support potential accelerated development pathways in recurrent CNS cancers.
Importantly, this represents the first clinical readout of NeOnc’s bioconjugated temozolomide (TMZ) platform in an oral formulation, demonstrating NeOnc’s drug-engineering capabilities beyond its established intranasal delivery platform. The data validate the Company’s ability to optimize CNS penetration and therapeutic exposure across both intranasal and oral modalities. NeOnc intends to request a Type B (End-of-Phase 1) FDA meeting to review safety, PK/PD, preliminary efficacy, RP2D justification, Phase 2 design modifications, and a potential Accelerated Approval pathway. Supporting regulatory materials, including MedWatch Form FDA 3500A and Form FDA 1571, have been submitted via eCTD, ensuring regulatory transparency and alignment as the program transitions into Phase 2 development.
Mr. Heshmatpour, continued:
“This clinical data readout represents a meaningful advancement relative to the historical standard of care in brain cancer, temozolomide (TMZ), originally developed by Merck (NYSE: MRK). Importantly, we have successfully engineered and clinically evaluated a bio-conjugated oral formulation of TMZ, NEO212, and have established the Recommended Phase 2 Dose (RP2D). Achieving dose confirmation is a critical milestone that substantially de-risks the program and positions us for the next stage of development.
We believe NEO212 has the potential to meaningfully improve upon conventional TMZ by enhancing therapeutic performance while maintaining the practicality of oral administration. With this milestone achieved, we are preparing to engage the U.S. Food and Drug Administration to align on the design of what we anticipate will be a pivotal, registrational Phase 2 study, subject to FDA feedback and approval.
If successful, this program could redefine the treatment paradigm for glioblastoma, astrocytoma, and other aggressive CNS malignancies.”
NEO212 is specifically designed to overcome a key biological limitation of TMZ: MGMT-mediated resistance. Preclinical studies have shown that NEO212 effectively inactivates and promotes the degradation of O6-methylguanine-DNA methyltransferase (MGMT), a crucial DNA repair enzyme that causes TMZ resistance. Standard TMZ treatment does not significantly lower MGMT levels and remains vulnerable to MGMT-driven DNA repair in brain tumors. This mechanistic difference may be especially important for TMZ-resistant and MGMT-high recurrent glioblastoma patients, offering a strong biological reason to advance NEO212 into Phase 2 development in the post-TMZ setting.
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Mr. Heshmatpour added:
“This marks our first clinical readout of a bio-conjugated oral oncology asset and validates the broader scientific foundation of our platform. Supported by approximately ten issued patents and patent applications across the NEO212 and NEO100 programs, we believe our intellectual property portfolio provides meaningful long-term strategic protection.
Our immediate priority is regulatory engagement and disciplined execution toward a pivotal registrational pathway. We remain focused on advancing differentiated CNS therapies that can create durable clinical value for patients and sustainable long-term value for shareholders.”
Founder, Dr. Thomas Chen, Vice-Chairman and Chief Medical Officer noted that, “The determination of the RP2D at 610 mg is a scientifically significant achievement. It confirms that our bio-conjugation technology allows for high-dose delivery of therapeutic agents with a manageable toxicity profile. We are now positioned to explore the efficacy of this optimized dose in our upcoming Phase 2 expansion.”
Dr. Henry Friedman of Duke University emphasized the importance of this milestone, stating, “Establishing a safe and tolerable dose is the foundation of any successful oncology program. The identification of the RP2D for NEO212 allows NeOnc to proceed with confidence into efficacy studies for a patient population in desperate need of new oral therapies.”
NEO212 is NeOnc’s first oral chemical conjugated chemotherapy drug, uniquely combining Temozolomide (TMZ), the current standard of care for glioblastoma and other brain cancers (marketed as Temodar®), with NEO100 (a proprietary form of perillyl alcohol (POH), which is owned and patented by NeOnc). This proprietary conjugation is designed to overcome the limitations of TMZ, including resistance and limited efficacy, by enhancing blood-brain barrier penetration and antitumor activity.
Conference Call Details:
| ● | Date: March 4, 2026 |
| ● | Time: 6:00 a.m. PT / 9:00 a.m. ET |
| ● | Webcast: A live webcast can be accessed at: https://www.webcaster5.com/Webcast/Page/3151/53708 or by visiting https://investors.neonc.com |
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ABOUT NEONC TECHNOLOGIES HOLDINGS, INC.
NeOnc Technologies Holdings, Inc. is a clinical-stage life sciences company focused on the development and commercialization of central nervous system therapeutics that are designed to address the persistent challenges in overcoming the blood-brain barrier. The company’s NEO™ drug development platform has produced a portfolio of novel drug candidates and delivery methods with patent protections extending to 2038. These proprietary chemotherapy agents have demonstrated positive effects in laboratory tests on various types of cancers and in clinical trials treating malignant gliomas. NeOnc’s NEO100™ and NEO212™ therapeutics are in Phase II human clinical trials and are advancing under FDA Fast-Track and Investigational New Drug (IND) status. The company has exclusively licensed an extensive worldwide patent portfolio from the University of Southern California consisting of issued patents and pending applications related to NEO100, NEO212, and other products from the NeOnc patent family for multiple uses, including oncological and neurological conditions.
For more about NeOnc and its pioneering technology, visit https://neonc.com
Important Cautions Regarding Forward Looking Statements
This press release contains “forward-looking statements” within the meaning of Section 27A of the Securities Act of 1933, as amended, and Section 21E of the Securities Exchange Act of 1934, as amended. These forward-looking statements can be identified by terminology such as “may,” “will,” “should,” “intend,” “expect,” “plan,” “budget,” “forecast,” “anticipate,” “believe,” “estimate,” “predict,” “potential,” “continue,” “evaluating,” or similar words. Statements that contain these words should be read carefully, as they discuss our future expectations, projections of future results of operations or financial condition, or other forward-looking information.
Examples of forward-looking statements include, among others, statements regarding whether the data validates the Company’s ability to optimize CNS penetration and therapeutic exposure across both intranasal and oral modalities and whether NEO212 has the potential to replace TMZ as the future standard of care for all brain cancers. These statements reflect our current expectations and beliefs based on information available at this time, but future events may differ materially from those anticipated.
The “Risk Factors” section of our Quarterly Report on Form 10-Q for the three months ended March 31, 2025 as filed with the Securities and Exchange Commission, along with other cautionary language in that report and risk factors and other cautionary language in our subsequent filings with the Securities and Exchange Commission, outlines important risks and uncertainties. These may cause our actual results to differ materially from the forward-looking statements herein, including but not limited to the fact that results of preclinical studies and early clinical trials may not be predictive of results of future clinical trials, announced or published data from our clinical trials may change as more patient data become available and are subject to audit and verification procedures that could result in material changes in the final data and our product candidates are in preclinical and clinical stages of development, are not approved for commercial sale and might never receive regulatory approval or become commercially viable.
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We assume no obligation to revise or update any forward-looking statements, whether as a result of new information, future developments, or otherwise, except as required by applicable securities laws and regulations.
“NEO100” and NEO “212” are registered trademarks of NeOnc Technologies Holdings, Inc.
Company Contact:
info@neonc.com
Investor Contact:
James Carbonara
Hayden IR
(646)-755-7412
james@haydenir.com
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Exhibit 99.2
Removing Barriers to Effective Neuro - Drug Delivery Corporate Presentation 202 6 NT HI Phase 1/2 Safety and Efficacy of NEO212 in Patients With Astrocytoma IDH - mutant, Glioblastoma IDH - wildtype or Brain Metastasis (NCT06047379)
Important Cautions Regarding Forward Looking Statements © NeOnc Technologies Holdings, Inc. 2022 - 2025. All Rights Reserved. Proprietary. 2 This document does not constitute or form part of an invitation or recommendation to subscribe for or purchase any securities. The distribution may be restricted by law in certain jurisdictions and persons into whose possession this document comes should inform themselves about, and observe, any such restriction. Any failure to comply with these restrictions may constitute a violation of the laws of any such jurisdiction. NeOnc Technologies Holdings, Inc. (“NeOnc”, “Company,” “our” or “ours”) shall not have any responsibility for any such violations. Any decision to purchase or subscribe for securities in any offering must be made solely on the basis of the information issued in connection with such offering. This document was prepared exclusively for the benefit and internal use of investors to evaluate the feasibility of a possible transaction or transactions and does not carry any right of publication or disclosure to any other party. This document is incomplete without reference to and should be viewed solely in conjunction with, the oral briefing provided by the Company. This presentation may not be used for any other purpose without the prior written consent of the Company. In preparing this document, we have relied upon and assumed, without independent verification, the accuracy and completeness of all information available from public sources or which was provided to us or otherwise reviewed by us. We do not represent that such information is accurate or complete, and it should not be relied on as such. Any opinions expressed herein reflect our judgment at this date, all of which are accordingly subject to change. We have based the forward - looking statements on our current expectations and projections about future events. These forward - looking statements are subject to known and unknown risks, uncertainties, and assumptions about us and our affiliate companies with respect to specific factors identified in this presentation and the Company’s filings with the U.S. Securities Exchange Commission, and which may cause our actual results, levels of activity, performance or achievements expressed or implied by such forward - looking statements differ materially from those currently anticipated in such statements. This presentation has been prepared by the Company for informational purposes only and not for any other purpose. This presentation shall not constitute an offer to sell or the solicitation of an offer to buy, nor shall there be any sale of securities in any jurisdiction in which such offer, solicitation or sale would be unlawful prior to the registration or qualification under the securities laws of any such jurisdiction. THIS PRESENTATION AND ANY OTHER INFORMATION THAT MAY BE FURNISHED BY US INCLUDES OR MAY INCLUDE CERTAIN STATEMENTS, ESTIMATES AND FORWARD - LOOKING PROJECTIONS OF THE COMPANY WITH RESPECT TO THE ANTICIPATED FUTURE PERFORMANCE OF THE COMPANY. SUCH STATEMENTS, ESTIMATES AND FORWARD - LOOKING PROJECTIONS REFLECT VARIOUS ASSUMPTIONS OF MANAGEMENT THAT MAY OR MAY NOT PROVE TO BE CORRECT AND INVOLVE VARIOUS RISKS AND UNCERTAINTIES.
Senior Management Team Board of Directors Scientific Advisory Board
Phase 2 Development & Clinical Pipeline 4 FDA Authorized Clinical Trials Commercialization Phase III Phase II Phase I IND Enabling * Preclinical Indication Application Drug Candidate Recurrent Grade III & Grade IV Astrocytoma Brain Cancer w/ IDH1 Mutation Intranasal NEO100 NEO100 - 01 Meningioma Brain Tumors Intranasal NEO100 NEO100 - 02 Pediatric Brain Tumors Intranasal NEO100 NEO100 - 03 All Brain Tumors Oral NEO212 NEO212 Phase 2 Phase 1** Our Clinical Pipeline Continues to Expand to Include Other Applications of NEO100 & NEO212 Important Disclaimer: This development & clinical pipeline is subject to regulatory approval, risk and uncertainties, as well as potential changes to the pipeline and other factors that are beyond our control. Phase 2 Registrational Trial Phase 2a **IND Enabling: Research to establish whether a compound is reasonably safe for initial use in humans and exhibits pharmacolo gic al activity that justifies commercial development.
5 GBM & Temozolomide (TMZ): Fundamental Limitations Bottom line: Temozolomide validated market demand in GBM; its clinical limitations inform the development rationale for NEO212 2nd - Line Recurrent Brain Tumor Benchmarks • Foundational standard of care since ~2005 , used with surgery and radiation; provides modest median OS benefit (~14 - 16 months), ~70 – 80% of patients experience tumor progression within 12 months • Widespread global adoption , with peak sales estimated at ~$3 – 4B, despite known limitations in the durability of response • MGMT promoter methylation (~35 – 45% of patients) is associated with increased TMZ sensitivity • Broad real - world use regardless of MGMT status , including in unmethylated tumors with reduced expected benefit • Systemic exposure to active metabolite (AIC) is associated with hematologic toxicity, including bone marrow suppression • Treatment - limiting myelosuppression may reduce dose intensity or duration, independent of tumor response • Median frontline PFS ~6 – 7 months , with progression observed in both methylated and unmethylated disease • Limited options post - progression , with salvage therapies providing variable benefit and a median survival of ~6 – 9 months following recurrence Key Trial Context OS - 12 (%) Median OS ( mo ) Therapy REGOMA (~20%); EORTC 26101 (~30 – 35%) ~20 – 35% 5.6 – 8.6 CCNU ( lomustine ) alone BRAIN Trial ~38 – 43% ~9.2 Bevacizumab (Avastin) alone EORTC 26101 ~35 – 40% ~9.1 CCNU + Bevacizumab* EF - 11 ~20 – 25% ~6.6 TTFields alone
NEO212: Brain - Optimized Temozolomide Bioconjugate Designed to Enhance Brain Tumor Targeting NEO100 Temozolomide (TMZ) Carbamide Bond NEO212 Bioconjugated Molecule 6 Novel bioconjugate combining NEO 100 with temozolomide (TMZ) . Builds on TMZ, the established GBM standard of care, with the goal of improving brain delivery and durability of response . Enhanced BBB penetration targets brain tumors more effectively than TMZ Dual - mechanism : Complementary activity from NEO 100 and TMZ in one molecule . Bioconjugation optimizes PK and CNS exposure Clinically ready for studies in primary and secondary malignant brain cancers, including GBM and brain metastases . Multiple delivery routes planned, with evaluation of both oral and intranasal administration .
7 NEO212 Degrades MGMT and Overcomes TMZ Resistance in GBM Chen TC et al. Cancer Lett. 2015 Mar 28;358(2):144 - 151. Cho HY et al. Neurooncol Adv. 2020 Nov 20;2(1):vdaa160. Cho HY et al Mol Cancer Ther. 2014 Aug;13(8):2004 - 17. NEO212 Achieves Higher Intratumoral TMZ/AIC Exposure in TMZ - Resistant GBM NEO212 degrades MGMT and Kills TMZ - Resistant GBM Without the Need for MGMT Inhibitor O⁶BG NEO212 Demonstrates Greater Cytotoxicity Than Temozolomide in Human GBM Cell Lines
8 NEO212 Demonstrates Enhanced Brain Delivery and Antitumor Activity in TMZ - Resistant GBM BBB penetration ↑ | Overall survival ↑ | Tumor size ↓ Chen TC et al. Cancer Lett. 2015 Mar 28;358(2):144 - 151. Cho HY et al. Neurooncol Adv. 2020 Nov 20;2(1):vdaa160. Cho HY et al Mol Cancer Ther. 2014 Aug;13(8):2004 - 17. Intracranial Xenograft Model Patient - derived USC - 02 MGMT + GBM ≈3 î Higher Brain - to - Serum Ratio Observed for NEO212 vs Temozolomide Increasing NEO212 Levels Observed in Tumor Tissue Along with Its Metabolites PA and AIC
NEO212 Mechanism of Action 9 Chen TC et al. Cancer Lett. 2015 Mar 28;358(2):144 - 151. Cho HY et al. Neurooncol Adv. 2020 Nov 20;2(1):vdaa160. Cho HY et al Mol Cancer Ther. 2014 Aug;13(8):2004 - 17.
NEO212: Novel Alkylating Therapy with Preclinical Evidence of MGMT Inactivation and Brain Penetration in Clinical Development for Brain Tumors 10 Broad Scope: Primary brain tumors and brain metastases as monotherapy and in combination with SOC Differentiation vs TMZ: Up to 10 î greater preclinical efficacy , including MGMT - positive (TMZ - resistant) tumors with NEO212 - Mediated MGMT Inactivation Safety Advantage: Lower systemic toxicity and myelosuppression vs TMZ Brain Delivery: 3 î higher BBB penetration (brain: serum ratio) vs TMZ Phase I (completed): Assessing safety, tolerability, and preliminary efficacy in primary brain tumors and solid - tumor brain metastases Strategic Opportunity: Designed to replace or augment TMZ across primary and metastatic brain cancer indications
Phase 1: Safety and Efficacy of NEO212 in Patients With Astrocytoma IDH - mutant, Glioblastoma IDH - wildtype or Brain Metastasis Phase 1: (dose escalation) Primary Objectives : • Assess the safety and tolerability of increasing dose levels of orally administered NEO212 alone in patients with Astrocyto ma IDH - mutant, Glioblastoma IDH - wildtype or patients with select solid tumors with uncontrolled metastases to the brain. • Identify the maximum tolerated dose (MTD) of NEO212. • Determine the recommended Phase 2 dose (RP2D) of NEO212. Secondary Objectives: • Characterize the pharmacokinetics (PK) of NEO212. • Evaluate anti - tumor activity of NEO212 in patients with Astrocytoma IDH - mutant, Glioblastoma IDH - wildtype and patients with select solid tumors with uncontrolled metastases to the brain. Total Subjects MGMT Status Tumor Type 3 N=1, Not applicable Squamous NSCLC - to - Brain Metastasis Cohort 1 (170mg/day) N=2 Methylated GBM IDH1 - wildtype 3 N=2 Methylated, N=1 Unmethylated GBM IDH1 - wildtype Cohort 2 (220mg/day) 3 N=1, Not applicable Esthesioneuroblastoma - to - Brain Metastasis Cohort 3 (400mg/day) N=1, Not applicable Breast - to - Brain Metastasis N=1, Methylated GBM IDH1 - wildtype 3 N=1 Equivocal1, N=1 Unmethylated, N=1 Methylated GBM IDH1 - wildtype Cohort 4 (610mg/day) 2 N=2 Methylated GBM IDH1 - wildtype Cohort 5 (810mg/day) NEO212 Phase 1 – Patient Distribution by Cohort Subjects received NEO212 orally once daily on Days 1 through 5 of each 28 - day treatment cycle.
12 Low Peripheral Blood Detection of NEO212 Metabolites (AIC and PA) in Phase 1 PK Samples, Consistent with Preclinical Observations of Tumor Uptake and Intratumoral Metabolism Cohort 5 (810 mg/QD) Cohort 4 (610 mg/QD) Cohort 3 (400 mg/QD) Cohort 2 (220 mg/QD) Cohort 1 (170 mg/QD) 2 3 3 3 3 N (evaluable) 3.25 16.8 12.19 2.52 1.94 Mean Peak AIC (ng/mL) 0 – 36.0 0 – 120.0 0 – 117.0 0 – 47.0 0 – 49.6 AIC Range (ng/mL) 6.96 13.83 2.04 0.07 0.17 Mean Peak PA (ng/mL) 0 – 43.6 0 – 80.2 0 - 21.2 0 - 12.5 0 - 27.7 PA Range (ng/mL) Cho et al, Neuro - Oncology Advances, 2020 These findings suggest reduced systemic metabolite exposure and potential enhanced tumor targeting, which may be associated with lower systemic toxicity compared with temozolomide.
13 39 î Lower AIC Levels Observed with NEO212 vs Temozolomide, Reflecting Reduced Systemic Metabolite Levels and Potentially Supporting an Improved Hematologic Safety Profile Fig . 4 Representative TMZ ( F ), MTIC ( E ), and AIC ( Ƒ ) concentra - tion - time profiles from a patient who received 200 mg of TMZ . Solid and dashed lines , best - fit curves from the model - estimated parameters . NEO212 TMZ Brain - adjusted exposure NEO212 vs TMZ 200 mg/m² (Cycle 2+) Brain - adjusted relative (3x BBB - permeable) Relative Exposure compared to TMZ TMZ total over 5 days (mg) NEO212 total 5 - day dose (TMZ - equivalent, mg; conversion ratio = 0.521) NEO212 total over 5 days (mg) NEO212 (mg/day) 0.73 0.25 1800 443 850 170 Cohort 1 0.93 0.32 1800 573 1,100 220 Cohort 2 1.69 0.58 1800 1,042 2,000 400 Cohort 3 2.56 0.88 1800 1,589 3,050 610 Cohort 4 3.40 1.17 1800 2,110 4,050 810 Cohort 5 cohort 5 cohort 4 cohort 3 cohort 2 cohort 1 6.62 24.01 20.54 6.29 3.91 Cmax (ng/ml) 3.25 16.78 12.19 2.52 1.94 Mean (ng/ml) 2.64 4.76 5.71 2.13 1.62 Std. Deviation 1.00 2.13 2.33 0.81 0.61 Std. Error of Mean 0.81 10.87 6.20 0.54 0.44 Lower 95% CI of mean 5.69 22.69 18.18 4.49 3.44 Upper 95% CI of mean Mean AIC 657ng/ml Adjusted for Body Weight, NEO212 Achieves Higher CNS Delivery vs. TMZ
NEO212 PK: No Clinically Meaningful Myelosuppression Detected
NEO212 PK: No Clinically Meaningful Hepatic or Renal/Urinary Toxicity Observed
16 MTD Cohort 5 (810 mg QD) – Key Learnings Observed SAEs were consistent with complications commonly seen in advanced recurrent GBM and during temozolomide - Phase 1 dose escalation studies. Importantly, across Phase 1: • No signal of clinically meaningful myelosuppression • No hepatic or renal toxicity signal This differentiates systemic safety profile from traditional TMZ - associated hematologic suppression. Brain - adjusted exposure NEO212 vs TMZ 200 mg/m² (Cycle 2+) Brain - adjusted relative (3x BBB - permeable) Relative Exposure compared to TMZ TMZ total over 5 days (mg) NEO212 total 5 - day dose (TMZ - equivalent, mg; conversion ratio = 0.521) NEO212 total over 5 days (mg) NEO212 (mg/day) 0.73 0.25 1800 443 850 170 Cohort 1 0.93 0.32 1800 573 1,100 220 Cohort 2 1.69 0.58 1800 1,042 2,000 400 Cohort 3 2.56 0.88 1800 1,589 3,050 610 Cohort 4 3.40 1.17 1800 2,110 4,050 810 Cohort 5
17 NEO212 measurable anti - tumor activity in Phase 1
18 Partial Response Observed in Recurrent IDH1 Wild - Type, MGMT - Methylated GBM – Patient Remains Stable 21 Months Post - Recurrence Screen Cycle 21 Contrast FLAIR Primary Diagnosis: 8/25/2023 Prior Tx: XRT+TMZ (10/23 - 4/24) Progressed on TMZ After 6 Cycles NEO212 C1D1: 6/10/2024 Currently on Cycle 22 of NEO212
19 Lung - to - Brain Metastasis | 55 Months Since Diagnosis | Last 16 Months on NEO212 Screen Cycle 7 Contrast FLAIR Brain Met Diagnosis: Squamous NSCLC (7/20/2021) Prior Tx: Taxol/Carboplatin (7/2018); Keytruda, Alimta (5/2020) NEO212 C1D1: 3/25/2024 Currently on Cycle 16
20 NEO212 — Next Potential Steps & Accelerated Regulatory Approval Phase I Readout: Initial safety, PK, and preliminary efficacy data Accelerated Approval Strategy: Advancement into Two Phase II Clinical Trials •Trial 1: Randomized evaluation of single - agent NEO212 in recurrent GBM versus standard - of - care therapy •Trial 2: Randomized evaluation of NEO212 in combination with standard - of - care therapy versus standard - of - care therapy alone in patients with brain metastases Unmet Need (Brain Mets): >30% of adult cancer patients develop brain metastases with no durable systemic standard of care TAM — Primary GBM: ~$3.0 - 4.0B estimated market opportunity TAM — Brain Metastases: Approximately 10x the size of the primary GBM market
NEO212: Phase 1 Clinical Data Informing an Accelerated Phase 2 Development Strategy in TMZ - Resistant Glioblastoma and Brain Metastases 1. Safety Foundation Established • Phase 1 demonstrated favorable systemic tolerability Why It Matters: Temozolomide’s dose ceiling is bone marrow suppression. NEO212 may enable sustained alkylator therapy without the traditional hematologic limitation. 2. Early Signals of Clinical Activity in Recurrent GBM • Durable disease control observed in heavily pretreated patients • Biological rationale supported by activity in TMZ - resistant, MGMT - high preclinical models • Designed to enhance brain delivery while preserving cytotoxic potency Why It Matters: ~70 – 80% of GBM patients progress within 12 months of TMZ. NEO212 is positioned to retain activity where TMZ fails. 3. Phase 2 Targets the Highest - Value Unmet Segment • Focus on MGMT - unmethylated and TMZ - refractory patients • Includes patients who discontinued TMZ due to hematologic toxicity • Randomized vs SOC for clean efficacy signal • ORR primary endpoint built for Accelerated Approval Why It Matters: Phase 2 directly tests NEO212 in the population most underserved by current standard therapy — resistance - driven and toxicity - limited patients.
THE FUTURE OF DRUG DELIVERY Company Contact NeOnc Technologies Holdings, Inc. 23975 Park Sorrento , Suite 205 Calabasas, CA 91302 Tel +1 (818) 470 - NTHI Info@neonc.com www.neonc.com Investor Relations Hayden IR 2369 Lexington Avenue , Second Floor New York, New York 10017 Brett Maas Managing Partner brett@haydenir.com James Carbonara Partner James@haydenir.com 646 - 755 - 7412 Contact Us 22
Exhibit 99.3
Transcript of
NeOnc Technologies Holdings, Inc.
Investor Conference Call to Present Dose-Escalation Results from Full Phase 1
NEO212-01 Readout for Dosing and Toxicity
March 4, 2026
Participants
Thomas Chen - Founder and Chief Medical Officer, NeOnc Technologies
Keithly Garnett - Chief Financial Officer, NeOnc Technologies
Josh Neman - Chief Clinical Officer, NeOnc Technologies
Henry Friedman - Scientific Chair, Scientific Advisory Board, NeOnc Technologies
Amir Heshmatpour - CEO, Executive Chairman, and President, NeOnc Technologies
Presentation
Thomas Chen - Founder and Chief Medical Officer, NeOnc Technologies
Good morning, everybody, my name is Dr. Thomas Chen. I’m the Founder and CMO of NeOnc Technologies. I am here to present to you our Phase 1 study, which is entitled Safety and Efficacy of NEO212 in Patients with Astrocytoma IDH1-mutant, Glioblastoma IDH1-wildtype or Brain Metastasis.
Over to you, Keithly.
Keithly Garnett - Chief Financial Officer, NeOnc Technologies
Good morning, allow me to introduce you to our company and our team. First, you can see that we have our safe harbor language presented. Our team today, we’re comprised of the senior management team, includes gentlemen to my right, Mr. Amir Heshmatpour, who serves as our Chief Executive Officer, Executive Chairman, and President. To his right, we have Dr. Thomas Chen, as he said, he’s the Founder, Chief Medical Officer, and practicing neurosurgeon. Next to him, we have Dr. Josh Neman, who serves as our Chief Clinical Officer. My name is Keithly Garnett, I serve as Chief Financial Officer. I’m also happy to welcome to our team a new addition by the name of [David Choi, who’s our Chief Accounting Officer] [ph].
As you can see, we have assembled a Board of Directors that is compliance with independent board members, and we also have a panel of scientific advisory board members, as you can see on the screen. We’re also joined today by the Chair of our Scientific Advisory Board, Dr. Henry Friedman.
With that, Dr. Chen will walk us through the slides.
Thomas Chen - Founder and Chief Medical Officer, NeOnc Technologies
Yes. Thank you, Keithly. So today, what I’m going to start off with is talk to you about our trials in progress, but mainly focus on NEO212, which is the toxicity studies that we want to present to you. We have three studies using NEO100-01. Those are our intranasal studies that are in progress. I just want to highlight a couple of things. NEO100-01 actually has finished recruiting for Phase 2a. We recruited 25 patients. We will be announcing the readout after in 5 months, in terms of the Phase 2a results. And then NEO100-02 is still in progress. It’s in Phase 2 for malignant and atypical meningiomas. And NEO100-03 is also given intranasally. It will be given for pediatric patients with malignant brain tumors that will be recruiting for Phase 1.
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Today, our focus is going to be NEO212, which is a drug that is a bio-conjugated product that we will be describing. And it’s given orally, and it was used for treating all brain tumors. So let me tell you a little bit about why we are interested in NEO212 and the unmet need that it is serving. First of all, you may know that temozolomide, a DNA alkylating agent, is used as the standard of care for chemotherapy in brain tumors today. And approximately in these brain tumor patients, these patients will all have progression within 12 months.
What we have been doing is observing some of the problems with temozolomide usage. And in my experience, we have two main problems. One is that this temozolomide only works in about 45% of the patients. And the reason why is because in order to have a DNA repair enzyme that is in there for temozolomide to be active, it needs to have a DNA repair enzyme called MGMT inactive. And therefore, about 45% of the patients are not responsive to temozolomide. We want to make a drug that could be used universally for all patients.
The other problem with temozolomide is myelosuppression. Temozolomide induces drops in the patient’s white count and platelet function that prevents it from long-term usage. These are the two main problems in my mind with temozolomide usage. This is the unmet need that we will be used to treating these patients.
So, I’m going to give you a very brief overview of why we think that this bio-conjugate is very effective. What you have here with our bio-conjugate is that we have a temozolomide, which is basically a prodrug. But we conjugate the temozolomide via a carbamide bond to NEO100. We stabilize temozolomide and make it much more effective. And the reason why it’s more effective is it gets across the blood-brain barrier better. The bio-conjugation stabilizes, enables more temozolomide to get to the tumor, and also prevents it from breaking down and causing mild toxicity.
I’m going to turn this presentation now over to Josh Neman, who’s going to talk to you a little bit about the science and the translational studies that were performed prior to this going to a Phase 1 study.
Josh Neman - Chief Clinical Officer, NeOnc Technologies
Thank you, Tom. I’m going to be going over our preclinical studies, which our R&D team has come up with over the years, and it’s all published data. The key thing with respect to NEO212 is that what we observe here is that in tumor cells, in GBM cells that have that MGMT enzyme, NEO212 works greater than temozolomide itself. This is done by basically deactivating or degrading the MGMT enzyme. This is something that temozolomide is not able to do, but NEO212 does.
When we look inside the cells of these tumors in these temozolomide-resistant cells, we can get a higher concentration of the temozolomide breakdown that comes from NEO212 compared to TMZ or temozolomide alone. Moreover, the active metabolite AIC is seen much greater inside these tumor cells than TMZ alone. In a head-to-head comparison of temozolomide versus NEO212 in various glioblastoma cell lines that are sensitive or not sensitive or resistant to temozolomide, what we see is that NEO212 in every instance has higher cytotoxicity than temozolomide alone. This translates from in vitro to in vivo cases as well.
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What we observe in vivo is that NEO212 has a greater blood-brain barrier penetration than temozolomide. This happens almost three-fold increase with respect to brain-to-serum ratios. Moreover, in our intracranial xenograft models of MGMT-positive tumor cells in a head-to-head comparison to temozolomide, NEO212 has significantly prolonged survival and also decreases tumor burden.
When we look inside the tissue of these cells in vivo, what we see is a greater concentration of NEO212 compared to the normal brain and the active metabolites AIC and the active stable metabolite of NEO100, which is perillic acid. We see increasing concentrations of this over time within tumor-bearing tissue in the brain. This is an overall schematic mechanism of NEO212. I just want to highlight here that, again, what NEO212 is able to do where TMZ fails is that it can degrade MGMT completely and it induces some ER stress, all leading to cytotoxicity of the tumor cell.
Overall, the broad scope of our trial and our goal is to become the standard of care therapy for primary brain tumors and brain metastasis. What differentiates us compared to temozolomide is that pre-clinically, we have up to 10x greater preclinical efficacy. This includes MGMT-positive TMZ-resistant tumors. As well as I just re-mentioned is that NEO212 mediates MGMT inactivation or degradation.
We’ve had lower systemic toxicity and myelosuppression compared to TMZ. We can deliver this chemotherapy 3 times higher into the brain through the blood-brain barrier. Our Phase 1s, which are now completed, which Tom will go over shortly, are going to assess safety, tolerability, and we will have preliminary anti-tumor activity in primary brain tumors and solid brain tumors.
So, I think going over the goal of our Phase 1, our Phase 1s are looking at safety and efficacy of NEO212 in patients with astrocytoma, IDH1 mutants, GPM IDH1 wild-types, or brain metastases. Our primary objectives were in this dose escalating trial where we got to look at safety and tolerability, identify the maximum tolerable dosage, and a recommended Phase 2 dosage, which we do now have.
Our secondary objective was to look at pharmacokinetics of NEO212 and evaluate any anti-tumor activity. What you see here in this table below is our dose escalating Cohorts from 1 through 5, our tumor types. As you can see, we have enrolled 14 patients. Of those, we’ve had IDH1 wild-type GBMs and various brain metastases. These subjects received the NEO212 orally once daily, days 1 through 5, on a 28-day treatment cycle. These were all pre-heavily treated patients who’ve had, who’ve failed temozolomide and were either in a recurrent state.
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What you can see here is our pharmacokinetic data looking at the metabolites of NEO212, which are the perillic acid, perillyl alcohol, and AIC. What I’d like you to appreciate is that these data are consistent with our preclinical observations of tumor uptake and intratumoral metabolism. These findings from our AIC and our perillic acid from Cohorts 1 through 5 show that the exposure levels of AIC and perillic acid are minimal. Therefore, again, consistently with our preclinical observation that the majority of the drug is taken up by the tumor cells.
If we do an adjusted body weight comparison of NEO212 compared to temozolomide, what we see is that NEO212 achieves higher CNS delivery compared to temozolomide from Cohorts 2 through 5. More importantly, if we look at the AIC components, which are key to myelosuppression, what we end up seeing is that compared to temozolomide from their Phase 1 data, that they had AIC levels of 657 nanograms per ml. However, at that recommended Cohort 4, which will be our Phase 2 dosage, what we see is the mean AIC level of only 16 nanograms per ml, showing that there’s a 39 times lower AIC levels observed in NEO212 versus temozolomide, reflecting a probability of almost 98% safety of NEO212 compared to temozolomide.
Now, I’d like to turn it back to Dr. Chen, which he’ll go over some of the Phase 1 readouts.
Thomas Chen - Founder and Chief Medical Officer, NeOnc Technologies
Thanks, Josh. So, what I want to do is show you in terms of what the actual data with our patients in Phase 1 from the standpoint of whether there’s any evidence of myelosuppression. What I have is plots on a patient-by-patient basis in terms of their platelet count, their red blood count, the white blood count. And what you can see here is that over time with treatment, that there was no decrease in platelets, hemoglobin, or white blood count, or red blood cell count.
In addition, what we did was that we monitored both renal function and liver function. The liver function was measured by AST and ALT, and then kidney function by creatinine and also specific gravity. Again, what you see is that there was no elevation in the liver function test and then no elevation in the creatinine level. So what we did was that we also reached Dose-Limiting Toxicity with the study. And what you can see here is the fact that we met Dose-Limiting Toxicity at Cohort 5.
And one of the things that I want to emphasize to you is that this drug is different from temozolomide. And the reason what we did was that we calculated by molar dosage of temozolomide versus NEO212, and also we calculated by the amount of exposure of temozolomide by the ability of this drug to penetrate the blood-brain barrier. At Cohort 5, we basically got up to 3.40 times that of temozolomide. And at Cohort 4, it’s lower at 2.5. So basically, what we have done in this study is that we have demonstrated that there’s no clinically meaningful myelosuppression that was observed, and we had no hepatic or renal toxicities.
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Now, as you know, with the Phase 1 study, our goal is to measure toxicity. But we were able to demonstrate evidence of anti-tumor activity in a primary brain tumor and also a metastatic brain tumor. And I want to present to you some of these studies. So this patient had a partial response. This patient was IDH1 wild-type MGMT-methylated glioblastoma. The patient had been through the Stupp protocol, which consists of surgery, radiation, and temozolomide. He was actually on temozolomide for six cycles, and he progressed. He then came on our study.
What you can see here on this is I divide up the screen, and after cycle 21, the screen on the left-hand side is basically his tumor that you can see as a contrast-enhanced white portion of this axial cut. And then over 21 cycles, you can see that basically the tumor has shrunk and is now about 60% of his original size. And I also included for you some flare images as well and also a graph showing the original size of the tumor and then the size of the tumor after treatment.
Now with the brain metastasis patient, we did the same thing. This is actually a patient of mine. He has a non-small cell carcinoma of brain metastasis. His tumor kept recurring despite repeat surgeries. I actually performed three craniotomies on him. And so he came to the study after the third craniotomy. And then what you can see on the screen side is this tumor, which was in his occipital lobe. That’s the white-enhancing area. And then after seven cycles of treatment, we had a destabilization of disease and reduction of his tumor size.
So, I want to tell you where we’re going with this. Basically, we feel that we have reached our Dose-Limiting Toxicity of four or five. We feel that we have established initial safety, PK, and preliminary efficacy data. What we’re trying to do is go into two Phase 2 clinical trials. We will be doing one clinical trial based on a randomized evaluation of single-agent NEO212 in recurrent GBM versus standard of care therapy. And the second trial will be a randomized evaluation of NEO212 in combination of standard of care therapy versus standard of care therapy alone in patients with brain metastases.
I want to emphasize to you that with brain metastases, this is truly an unmet need. Currently, all we have for these patients are surgery and radiation therapy, including radial surgery. And this allows us now to add chemotherapy as an additional adjunct therapy for these brain metastases.
So in terms of NEO212, some of the things that I’ve mentioned before, but I want to re-emphasize. One, this is a Phase 1 study. We’re looking for toxicity. And what we have been able to show you is that at dosages that are actually greater than the amount of temozolomide that’s given, we do not observe bone marrow suppression. This is truly unique compared to what temozolomide induces. And NEO212 may be able to have sustained alkylator therapy without the traditional hematologic limitation.
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The second thing is that even though this is a Phase 1 trial, we do have early signals of clinical activity in recurrent glioblastoma. Basically, what we have shown is that even though 70% to 80% of glioblastoma patients’ progress within 12 months of temozolomide, our drug is potentially be able to work on these patients. So what we want to do in position NEO212 to treat these patients and demonstrate that it retains activity where temozolomide fails.
So the Phase 2 study, again, it’s going to target the highest value unmet segment. And these are going to be focused on patients that are MGMT unmethylated, which means that temozolomide is not effective, and also with temozolomide refractory patients. We’re going to include patients with discontinued temozolomide due to hematological toxicity, because we believe that our drug does not induce that. It’s going to be a randomized versus standard care for clean efficacy signal. And we’re going to look at our primary endpoint for overall survival for accelerated approval.
Why this matters is because, again, we are meeting an unmet need in these temozolomide failure patients that have now induced resistance, and also temozolomide failure patients because they have toxicity.
Now, what I’d like to do is turn it over to Dr. Henry.
Keithly Garnett - Chief Financial Officer, NeOnc Technologies
We’d like to turn it now over to Dr. Henry Friedman, who’s the chair of our Scientific Advisory Board, for a few comments. Thank you.
Henry Friedman - Scientific Chair, Scientific Advisory Board, NeOnc Technologies
Okay. So, Dr. Chen is spot on that the single biggest problem with temozolomide sustained activity in GBM is MGMT, although there are a couple of other mechanisms of resistance, by far the most problematic one is MGMT. And a lot of different trials have been done, or preclinical and clinical efforts have been done, to try to overcome that resistance. I did trials with O6-benzylguanine in the clinic and in the preclinical situation, and the problem was the enhanced myelosuppression. So to have someone or some company have an ability to modulate temozolomide in the MGMT-positive tumors without an increase in any systemic toxicity, particularly bone marrow suppression or myelosuppression, is a pivotal step forward.
Temozolomide is one of the few drugs approved for standard of care for glioblastoma. The use of anything which can overcome MGMT-mediated resistance will be a game changer, and if this moves forward in the studies or other studies we’ve been talking about that can make this point, it will redefine the standard of care globally. So that this is a major step forward for patients with GBM, and it is important for us to really show that we can treat patients’ refractory to temozolomide and not increase the toxicity while restoring sensitivity. This has the potential to be an enormously popular and positive step forward in treating GBM.
I’m eager to see the results of the trials that are going to be coming.
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Amir Heshmatpour - CEO, Executive Chairman, and President, NeOnc Technologies
Thank you, Dr. Friedman. This is the conclusion of our investors call, but I’d like to just do a closing statement here. You just heard our management team present the data for our dosing and toxicity for our first bio-conjugated oral TMZ with NEO100. We have 179 patents worldwide. 10 of those patents protect this drug for us. Data that you heard was significantly better than the current standard of care that has an addressable market between $3 billion to $4 billion. We feel that we will become the addressable market leader with NEO212.
With that said, in the next 8 quarters, we are anticipating to run our pivotal registrational trials. We will be meeting with the FDA here in the next 2 to 4 weeks, coming up with the trial protocol and we will be disclosing that to the investors very shortly.
With that said, I thank everyone for coming to this meeting and hope to see you guys soon on our next investors meeting. Take good care and thank you.
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FAQ
What did NeOnc Technologies (NTHI) report from the Phase 1 trial of NEO212?
What is the Recommended Phase 2 Dose (RP2D) for NEO212 announced by NTHI?
How does NEO212 differ from standard temozolomide in NeOnc’s data?
What safety profile did NEO212 show in NeOnc Technologies’ Phase 1 study?
What are NeOnc Technologies’ next development plans for NEO212 after Phase 1?
Which patient populations were included in NeOnc’s NEO212 Phase 1 dose-escalation trial?
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