On April 10, 2022 Triumvira Immunologics ("Triumvira"), a clinical-stage company developing novel, targeted autologous and allogeneic T cell therapeutics that co-opt the natural biology of T cells to treat patients with solid tumors, reported it will present two posters at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting, taking place April 8-13, 2022 in New Orleans (Press release, Triumvira Immunologics, APR 10, 2022, View Source [SID1234611850]). The company will present an update from its ongoing TACTIC-2 clinical trial evaluating TAC01-HER2 in patients with HER2-positive solid tumors and new preclinical proof-of-concept data for its gastric cancer candidate, TAC-Claudin 18.2 (CLDN18.2).

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Triumvira’s TAC-T cell therapies feature TAC receptors that interact with the natural T cell receptor to uniquely help T cells recognize and eliminate cancer cells. They are designed to target specific cancer signatures, like HER2 and CLDN18.2. HER2 is commonly overexpressed in various solid tumors, including breast, ovarian and non-small cell lung cancers. CLDN18.2, by similar fashion, is a promising and reliable antigen selectively expressed on the surface of gastric tumor cells.

"We are very encouraged by the current progress of our clinical trial for TAC01-HER2, which has generated high levels of interest and momentum shown by the growing number of participating sites and noticeable increase in patient screening and enrollment by our investigators," said Deyaa Adib, M.D., Chief Medical Officer of Triumvira. "This will enable us to discuss patient data over the coming months at major cancer conferences in the USA and Europe."

"Our new preclinical evidence bolsters the viability of targeting CLDN18.2 and further demonstrates the versatility of our TAC platform for difficult-to-treat cancers," said Andreas Bader, Ph.D., Chief Scientific Officer of Triumvira. "We plan to build on this success through an eventual IND filing for CLDN18.2 and look forward to expanding our novel platform to address additional targets."

Update on TACTIC-2 study

Triumvira will provide an update on its ongoing TACTIC-2 Phase 1/2 multicenter, open-label trial designed to evaluate the safety, tolerability and efficacy of TAC01-HER2 in patients with HER2-positive solid tumors. Recruitment is ongoing across four sites in the U.S. and Canada as Triumvira plans to enroll approximately 135 participants in total. Patient cohort 1 dose level has completed enrollment and treatment with TAC-T cell therapy and met the requirements for evaluation of dose-limiting toxicities. In addition, the data safety monitoring committee completed its review of safety data from cohort 1, and recommended initiating enrollment for cohort 2.

Session: PO.CT01.04 – Phase I Trials in Progress 2
Presentation Title: CT247 / 8 – A phase I/II trial investigating safety and efficacy of autologous TAC T cells targeting HER2 in relapsed or refractory solid tumors (TACTIC-2)
Date: April 13, 2022, 9:00 AM – 12:30 PM CT
Location: Section 35

TAC-Claudin 18.2 demonstrates strong and specific activity against CLDN18.2-expressing solid tumor models

In the preclinical study of CLDN18.2, strong and specific activity of TAC-T cells targeted against CLDN18.2 was shown through a variety of in vitro assays, including demonstrated TAC-T cell activation in target cells expressing CLDN18.2. Lack of activity and increases in cytokine levels were observed in control settings, indicating that the T cell response is specific to the CLDN18.2 antigen. In addition to positive in vitro results, intravenous administration of CLDN18.2-TAC T cells led to sustained anti-tumor responses in various in vivo CLDN18.2 mouse models.

Session: PO.IM02.02 – Adoptive Cell Therapy 2
Presentation Title: 572 / 7 – Pre-clinical evaluation of Claudin 18.2 TAC T cells for the treatment of gastric cancer
Date: April 10, 2022, 1:30 – 5:00 PM CT
Location: Section 37

On April 10, 2022 Affimed N.V. (Nasdaq: AFMD) ("Affimed", or the "Company"), a clinical-stage immuno-oncology company committed to giving patients back their innate ability to fight cancer, reported a data update from the ongoing study of the Company’s lead innate cell engager (ICE) AFM13 precomplexed with cord blood-derived natural killer (cbNK) cells (Press release, Affimed, APR 10, 2022, View Source [SID1234611846]). AFM13 is currently being investigated at The University of Texas MD Anderson Cancer Center in a phase 1/2 study in patients with CD30-positive relapsed or refractory Hodgkin and non-Hodgkin lymphomas. The investigator-sponsored study is led by Yago Nieto, M.D., Ph.D., professor of Stem Cell Transplantation and Cellular Therapy at MD Anderson. The study shows a 100% objective response rate (ORR) and an improvement of complete response (CR) rate to 62% at the recommended phase 2 dose (RP2D) in 13 patients after 2 cycles of therapy. The results will be presented today during the Clinical Plenary Session on cellular immunotherapies at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2022 and will also be covered during an AACR (Free AACR Whitepaper) press conference this morning.

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"The data that we report today are highly encouraging. All patients on this trial were refractory to all available treatment options. Still the combination of AFM13 and precomplexed NK cells resulted in a 100% response rate and a 62% rate of complete responses. We are excited to see a deepening of responses from partial responses to complete responses with a second cycle and have amended the study to allow patients to receive additional cycles, which may further increase the efficacy," said Dr Andreas Harstrick, Chief Medical Officer at Affimed. "To our knowledge, this is the highest response rate reported so far in Hodgkin Lymphoma patients with treatment refractory disease."

As of the cut-off date, the study had enrolled 22 patients with relapsed or refractory CD30+ Hodgkin and non-Hodgkin lymphoma having received a median of seven prior lines of therapy, of whom 19 were evaluable for response. Thirteen response-evaluable patients were treated at the RP2D, including 12 patients with Hodgkin Lymphoma and one patient with non-Hodgkin Lymphoma. Each treatment cycle consists of lymphodepleting chemotherapy with fludarabine and cyclophosphamide followed two days later by a single infusion of cytokine-preactivated and expanded cord blood-derived NK cells that are pre-complexed with AFM13. Three weekly infusions of AFM13 (200 mg) monotherapy are subsequently administered and responses are assessed by the investigator on day 28 by FDG-PET.

All 13 patients treated at the recommended phase 2 dose (108 NK/Kg) achieved a response by Lyric criteria. Of these 13 patients, 8 patients (62%) demonstrated a CR after two cycles of treatment, which represents an increase from 5 patients (38%) demonstrating CR after one cycle of treatment previously announced in December 2021.

For the 13 patients treated at the RP2D, median duration of response has not yet been reached. As of the cutoff date, assessment of durability shows:

Seven patients remain in CR at median follow-up of 6.5 months, including two patients who remain in response after 10 months and two patients who received stem cell transplant and remain in response at 6.5 months
One patient with a CR experienced disease progression after 7.9 months
Of the five patients with a PR, one remains in response at 6.3 months and four patients progressed between 2.9 and 4.3 months after initial infusion
The treatment was well tolerated, with minimal side effects beyond the expected myelosuppression from the preceding lymphodepleting chemotherapy. No instances of cytokine release syndrome, immune effector cell-associated neurotoxicity syndrome, or graft versus host disease were observed. There were six infusion-related reactions in 110 infusions (5.4%) of AFM13 alone and no reactions to the cord blood-derived NK cells precomplexed with AFM13.

"A year ago, we were struck with hopeful optimism when the first four patients in the study all showed a response. Now, we are again presenting data at AACR (Free AACR Whitepaper) and the results not only hold strong in a larger patient population but also show an increasing number of CRs with early but encouraging durability," commented Dr. Adi Hoess, Chief Executive Officer at Affimed. "These ongoing successes with AFM13 represent an important milestone for Affimed and could mark a turning point in the innate immuno-oncology space, potentially setting the stage for expanding this approach to additional cancer indications. Our goal is to leverage the distinct features of our ROCK platform to generate best-in-class ICE molecules that drive effective innate immune cell activation for the benefit of broad patient populations, addressing hematologic and solid tumor malignancies."

The trial was originally designed to include up to two cycles. To assess durability beyond two cycles, an amendment has been approved by the U.S. Food and Drug Administration to increase the length of treatment from two up to four cycles, enabling longer follow up of patients.

AFM13, a bispecific tetravalent ICE molecule, is designed for high affinity binding, both to CD16A on NK cells and macrophages, and to CD30 on lymphoma cells. AFM13 is also being investigated as a monotherapy and can bind the patient’s own NK cells, thus boosting their existing capacity to fight cancerous cells. When precomplexed with AFM13, NK cells exhibit immediate expansion in the patient’s circulation which persists for at least two weeks.

Oral presentation details

Title: Innate cell engager (ICE) AFM13 combined with preactivated and expanded cord blood (CB)-derived NK cells for patients with refractory/relapsed CD30+ lymphoma

Presentation: CT003

Session: Clinical Trials of Cellular Immunotherapies, Sunday, April 10, 1:00 – 3:00 p.m. CST

About the Phase 1/2 Study

The University of Texas MD Anderson Cancer Center is studying AFM13 in an investigator-sponsored Phase 1/2 trial in combination with cord blood-derived allogeneic NK cells in patients with recurrent or refractory CD30-positive lymphomas. The study is a dose-escalation trial of pre-complexed NK cells, with patients receiving 1×106 NK cells/kg in Cohort 1; 1×107 NK cells/kg in Cohort 2; and 1×108 NK cells/kg in Cohort 3. The trial is designed to explore safety and activity and determine the recommended Phase 2 dose. In each cohort, the dose of the pre-complexed NK cells with AFM13 is to be followed by weekly doses of 200 mg AFM13 monotherapy for three weeks, with each patient evaluated for dose-limiting toxicities and responses on day 28.

MD Anderson has an institutional financial conflict of interest with Affimed related to this research and has therefore implemented an Institutional Conflict of Interest Management and Monitoring Plan.

Additional information about the study can be found at www.clinicaltrials.gov (NCT04074746).

About AFM13

AFM13 is a first-in-class innate cell engager (ICE) that uniquely activates the innate immune system to destroy CD30-positive hematologic tumors. AFM13 induces specific and selective killing of CD30-positive tumor cells, leveraging the power of the innate immune system by engaging and activating natural killer (NK) cells and macrophages. AFM13 is Affimed’s most advanced ICE clinical program and is currently being evaluated as a monotherapy in a registration-directed trial in patients with relapsed/refractory peripheral T-cell lymphoma or transformed mycosis fungoides (REDIRECT). Additional details can be found at www.clinicaltrials.gov (NCT04101331).

On April 10, 2022 Amgen (NASDAQ: AMGN) reported the presentation of long-term efficacy and safety data from the CodeBreaK 100 Phase 1/2 trial in patients with KRAS G12C-mutated advanced non-small cell lung cancer (NSCLC) who received LUMAKRAS (sotorasib)* (Press release, Amgen, APR 10, 2022, View Source [SID1234611830]). The two-year follow-up data will be presented orally as part of a clinical trials plenary session at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) annual meeting on April 10, 2022. LUMAKRAS is the first and only KRASG12C inhibitor to-date to show long-term clinical benefit and overall survival in patients with NSCLC harboring the KRAS G12C mutation.

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"With regulatory approvals in nearly 40 countries and thousands of patients treated, LUMAKRAS, the only approved KRASG12C inhibitor, is a transformative targeted therapy for the treatment of patients living with KRAS G12C-mutated NSCLC," said David M. Reese, M.D., executive vice president of Research and Development at Amgen. "We are pleased with these latest results from the CodeBreaK 100 study, which represent the longest follow-up of patients treated with a KRASG12C inhibitor and confirm rapid, deep and durable responses in patients receiving LUMAKRAS."

In this long-term, two-year analysis of 174 heavily pre-treated patients (172 with baseline measurable lesion(s)), LUMAKRAS demonstrated a centrally confirmed objective response rate (ORR) of 40.7%, disease control rate (DCR) of 83.7% and median duration of response (DOR) of 12.3 months. Five patients achieved complete responses and 65 patients achieved partial responses. The results also showed median progression-free survival (PFS) of 6.3 months and overall survival (OS) of 12.5 months with 32.5% of patients still alive at two years. No new safety signals for LUMAKRAS were identified with the long-term follow-up.

"Since the FDA approval almost a year ago, LUMAKRAS has changed the treatment paradigm for patients with advanced non-small cell lung cancer who harbor the KRAS G12C mutation," said Grace Dy, M.D., chief, thoracic oncology, Roswell Park Comprehensive Cancer Center. "The durable efficacy and positive benefit-risk profile seen in the two-year analysis of CodeBreaK 100 highlight the important role this innovative targeted therapy can offer long-term."

In May 2021, LUMAKRAS was the first KRASG12C inhibitor to receive regulatory approval with its approval in the U.S., under accelerated approval. LUMAKRAS is now approved in 39 countries.

*LUMAKRAS is marketed as LUMYKRAS (sotorasib) in the European Union, the United Kingdom and Switzerland.

About LUMAKRAS/LUMYKRAS (sotorasib)
Amgen took on one of the toughest challenges of the last 40 years in cancer research by developing LUMAKRAS/LUMYKRAS, a KRASG12C inhibitor.1 LUMAKRAS/LUMYKRAS has demonstrated a positive benefit-risk profile with rapid, deep, and durable anticancer activity in patients with locally advanced or metastatic non-small cell lung cancer (NSCLC) harboring the KRAS G12C mutation with a once daily oral formulation.2

Amgen is progressing the largest and broadest global KRASG12C inhibitor development program with unparalleled speed and exploring more than 10 sotorasib combination regimens, including triplets, with clinical trial sites spanning five continents. To date, over 4,000 patients around the world have received LUMAKRAS/LUMYKRAS through the clinical development program and commercial use.

In May 2021, LUMAKRAS was the first KRASG12C inhibitor to receive regulatory approval with its approval in the U.S., under accelerated approval. LUMAKRAS/LUMYKRAS is also approved in the European Union, Japan, United Arab Emirates, South Korea and Switzerland and in Australia, Brazil, Canada, and Great Britain under the FDA’s Project Orbis. Through Project Orbis, Amgen also has Marketing Authorization Applications (MAAs) for sotorasib in review in Israel and Singapore. Additionally, Amgen has submitted MAAs in Argentina, Colombia, Hong Kong, Kuwait, Malaysia, Mexico, Qatar, Saudi Arabia, Taiwan, Thailand and Turkey.

LUMAKRAS/LUMYKRAS is also being studied in multiple other solid tumors.3

About Non-Small Cell Lung Cancer and the KRAS G12C Mutation
Lung cancer is the leading cause of cancer-related deaths worldwide, and it accounts for more deaths worldwide than colon cancer, breast cancer and prostate cancer combined.4 Overall survival rates for NSCLC are improving but remain poor for patients with advanced disease and 5-year survival is only 7% for those with metastatic disease.5

KRAS G12C is the most common KRAS mutation in NSCLC.6 About 13% of patients with NSCLC harbor the KRAS G12C mutation.7 Unmet medical need remains high and treatment options are limited for NSCLC patients with the KRAS G12C mutation whose first-line treatment has failed to work or has stopped working. The outcomes with other approved therapies are suboptimal, with a median progression-free survival of approximately four months following second-line treatment of KRAS G12C-mutated NSCLC.8

About CodeBreaK
The CodeBreaK clinical development program for Amgen’s drug sotorasib is designed to study patients with an advanced solid tumor with the KRAS G12C mutation and address the longstanding unmet medical need for these cancers.

CodeBreaK 100, the Phase 1 and 2, first-in-human, open-label multicenter study, enrolled patients with KRAS G12C-mutant solid tumors.9 Eligible patients must have received a prior line of systemic anticancer therapy, consistent with their tumor type and stage of disease. The primary endpoint for the Phase 2 study was centrally assessed objective response rate. The Phase 2 trial in NSCLC enrolled 126 patients, 124 of whom had centrally evaluable lesions by RECIST at baseline.2 The Phase 2 trial in colorectal cancer (CRC) is fully enrolled and results have been published.10

CodeBreaK 200, the global Phase 3 randomized active-controlled study comparing sotorasib to docetaxel in KRAS G12C-mutated NSCLC completed enrollment of 345 patients. Eligible patients had previously treated, locally advanced and unresectable or metastatic KRAS G12C-mutated NSCLC. The primary endpoint is progression-free survival and key secondary endpoints include overall survival, objective response rate, and patient-reported outcomes.11

Amgen also has several Phase 1b studies investigating sotorasib monotherapy and sotorasib combination therapy across various advanced solid tumors (CodeBreaK 101) open for enrollment.12 A Phase 2 randomized study will evaluate sotorasib in patients with stage IV KRAS G12C-mutated NSCLC in need of first-line treatment (CodeBreaK 201).13

For information, please visit www.hcp.codebreaktrials.com.

LUMAKRAS (sotorasib) U.S. Indication
LUMAKRAS is indicated for the treatment of adult patients with KRAS G12C-mutated locally advanced or metastatic non-small cell lung cancer (NSCLC), as determined by an FDA-approved test, who have received at least one prior systemic therapy.

This indication is approved under accelerated approval based on overall response rate (ORR) and duration of response (DOR). Continued approval for this indication may be contingent upon verification and description of clinical benefit in a confirmatory trial(s).

LUMAKRAS (sotorasib) Important U.S. Safety Information

Hepatotoxicity

LUMAKRAS can cause hepatotoxicity, which may lead to drug-induced liver injury and hepatitis.
Among 357 patients who received LUMAKRAS in CodeBreaK 100, hepatotoxicity occurred in 1.7% (all grades) and 1.4% (Grade 3). A total of 18% of patients who received LUMAKRAS had increased alanine aminotransferase (ALT)/increased aspartate aminotransferase (AST); 6% were Grade 3 and 0.6% were Grade 4. In addition to dose interruption or reduction, 5% of patients received corticosteroids for the treatment of hepatotoxicity.
Monitor liver function tests (ALT, AST and total bilirubin) prior to the start of LUMAKRAS every 3 weeks for the first 3 months of treatment, then once a month or as clinically indicated, with more frequent testing in patients who develop transaminase and/or bilirubin elevations.
Withhold, dose reduce or permanently discontinue LUMAKRAS based on severity of adverse reaction.
Interstitial Lung Disease (ILD)/Pneumonitis

LUMAKRAS can cause ILD/pneumonitis that can be fatal. Among 357 patients who received LUMAKRAS in CodeBreaK 100, ILD/pneumonitis occurred in 0.8% of patients, all cases were Grade 3 or 4 at onset, and 1 case was fatal. LUMAKRAS was discontinued due to ILD/pneumonitis in 0.6% of patients.
Monitor patients for new or worsening pulmonary symptoms indicative of ILD/pneumonitis (e.g., dyspnea, cough, fever). Immediately withhold LUMAKRAS in patients with suspected ILD/pneumonitis and permanently discontinue LUMAKRAS if no other potential causes of ILD/pneumonitis are identified.
Most Common Adverse Reactions

The most common adverse reactions ≥ 20% were diarrhea, musculoskeletal pain, nausea, fatigue, hepatotoxicity and cough.
Drug Interactions

Advise patients to inform their healthcare provider of all concomitant medications, including prescription medicines, over-the-counter drugs, vitamins, dietary and herbal products.
Inform patients to avoid proton pump inhibitors and H2 receptor antagonists while taking LUMAKRAS.
If coadministration with an acid-reducing agent cannot be avoided, inform patients to take LUMAKRAS 4 hours before or 10 hours after a locally acting antacid.
Please see LUMAKRAS full Prescribing Information.

About Amgen Oncology
At Amgen Oncology, our mission to serve patients drives all that we do. That’s why we’re relentlessly focused on accelerating the delivery of medicines that have the potential to empower all angles of care and transform lives of people with cancer.

For the last four decades, we have been dedicated to discovering the firsts that matter in oncology and to finding ways to reduce the burden of cancer. Building on our heritage, Amgen continues to advance the largest pipeline in the Company’s history, moving with great speed to advance those innovations for the patients who need them.

At Amgen, we’re advancing oncology at the speed of life.

On April 9, 2022 PIC Therapeutics, Inc., a biotechnology company pioneering the discovery and development of first-in-mechanism, first-in-class allosteric therapies targeting eIF4E, reported it will present pre-clinical data on the company’s eIF4E program for ER+ breast cancer in a poster at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2022, taking place April 8-13, 2022 in New Orleans, LA (Press release, PIC Therapeutics, APR 9, 2022, View Source [SID1234611849]).

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"The preclinical results highlighted in this poster underscore the unique therapeutic advantages of allosterically modulating eIF4E and further demonstrate its potential as a promising strategy for patients with ER+ breast cancer," said Kathy Bowdish, Ph.D., president and chief executive officer of PIC Therapeutics.

PIC Therapeutics is targeting a fundamental mechanism at the convergence of many oncogenic signaling pathways, and results in cancer cell death while sparing normal cells. Allosteric modulation of eIF4E offers many advantages to previous approaches, and simultaneously addresses multiple drivers of pharmacology, allowing our small molecules to truly drive differential CAP dependent translation in target cells.

Importantly, preclinical studies show that PIC compounds modulate, but do not block protein translation. Consistently, our data demonstrate that as many proteins are upregulated as are downregulated as we alter protein complex membership. In ER+ breast cancer lines, PIC compounds upregulate a number of proteins responsible for apoptosis induction, including increases in caspase 3/7 activity along with demonstrated Annexin V binding, while simultaneously downregulating proteins involved in DNA repair. PIC compounds mechanistically modulate cellular proteomes, leading to rapid and significant reduction in cancer cell viability via apoptosis. Inducing apoptosis rather than senescence is an important distinguishing feature of PIC’s approach to this elusive target.

In ER+ breast cancer models, we observe evidence of mechanistic impacts in specific protein biomarkers with PICRN1024, PIC’s lead compound. Specifically aligned with patient data, we observe significant negative impacts on ERα expression, Cyclin D1 expression, CDK4 protein expression and decreases in the level of phospho-Rb. This mechanistic pharmacology helps us understand our impact on cell cycle transitions and correlates with decreases in ER+ breast cancer cell viability. Importantly, we also see simultaneous impacts on multiple mechanisms of breast cancer drug resistance including loss of PTEN, loss of Rb, CDK2, cyclin E, among others. Each of these impacts represent anticipated molecular profiles of ER+ Advanced Metastatic Breast Cancer patient tumors that have developed resistance to CDK4/6 inhibitors.

PIC Therapeutics is therefore uniquely positioned to therapeutically address eIF4E as one of the key drivers of cancer cell survival, uncovering unique mechanisms that may be harnessed for ER+ breast cancer patient benefit, with potential to expand more broadly across other oncology indications.

Presentation details are as follows:

Title: eIF4E modulators to address breast cancer resistance
Session Category: Experimental and Molecular Therapeutics
Session Title: Cell Cycle, Replication Inhibitors, and Immunotherapy Agents
Session Date and Time: April 12, 2022, 9:00 AM – 12:30 PM CT
Location: New Orleans Convention Center, Exhibit Hall D-H, Poster Section 21
Abstract Number: 2562

On April 9, 2022 Rhizen Pharmaceuticals AG (Rhizen), a Switzerland-based privately held, clinical-stage oncology & inflammation-focussed biopharmaceutical company, reported the release of data on its differentiated next-generation clinical-stage PARP (Poly ADP-Ribose Polymerase) and DHODH (DiHydro Orotate DeHydrogenase) inhibitor programs at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) 2022 Annual Meeting (Press release, Rhizen Pharmaceuticals, APR 9, 2022, View Source [SID1234611848]). Rhizen’s poster presentations describe the preclinical characterization and differentiated features of its novel PARP inhibitor (RP12146) and preclinical data supporting the broad positioning of its DHODH inhibitor (RP7214) in AML.

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Rhizen had earlier indicated that its PARP program had demonstrated differentiated IND enabling preclinical safety. The additional preclinical data being presented at AACR (Free AACR Whitepaper) 2022 suggests that this differentiated safety may be due to the lower bone marrow distribution of RP12146 and concomitantly lower haematological toxicity. "We believe RP12146’s safety differential has allowed us to progress through the dose escalation study more efficiently. Further, the emerging data from our ongoing phase 1 dose escalation study is encouraging & corroborative with robust target engagement and safety observed so far. We believe that this differentiation, as it translates more fully in the clinic, may allow us to explore the full potential of PARP inhibition across indications given RP12146’s potentially wide therapeutic window," said Swaroop Vakkalanka, Founder & CEO of Rhizen Pharma.

Rhizen indicated that its DHODH inhibitor, RP7214 has robust activity as a single agent in inducing tumor volume & size reduction and differentiation of AML blasts consistent with its mechanism of action. RP7214 also potentiates the activity of standard of care AML agents such as cytarabine, venetoclax and azacytidine. Swaroop added that "We have initiated a phase 2 study to explore RP7214 in combination with azacytidine in relapsed/refractory AML, CMML and MDS patients. The potential of DHODH inhibition as a therapeutic modality in AML remains unfulfilled and we expect RP7214 can eventually realize that potential. We believe elderly patients who are ineligible for frontline chemotherapy and maintenance settings represent areas of unmet need that RP7214 can address."

Details on Rhizen Pharma’s posters at AACR (Free AACR Whitepaper) are as follows:

Abstract Number: 1762
Title: Activity of RP7214, a novel, selective, and potent small molecule inhibitor of DHODH, in AML
Session: Small Molecule Therapeutic Agents
Poster Number: 5492
Abstract Number: 1766
Title: Activity of RP12146, a novel, selective, and potent small molecule inhibitor of PARP 1/2, in solid tumors
Session: Small Molecule Therapeutic Agents
Poster Number: 5493