Omeros Corp (OMER) 2023 Q2 法說會逐字稿

Good morning, and welcome to today's earnings call for Omeros Corporation. (Operator Instructions) Please be advised that today's call is being recorded at the company's request, and a replay will be available on the company's website for 1 week from today. I'll turn the call over to Jennifer Williams, Investor Relations for Omeros.

早上好，歡迎參加今天的 Omeros Corporation 財報電話會議。 （操作員說明）請注意，今天的通話是應公司要求進行錄音的，從今天起 1 週內將在公司網站上提供重播。我會將電話轉給 Omeros 投資者關係部門的 Jennifer Williams。

Good morning, and thank you for joining the call today. I'd like to remind you that some of the statements that will be made on the call today will be forward-looking. These statements are based on management's beliefs and expectations as of today only and are subject to change. All forward-looking statements involve risks and uncertainties that could cause the company's actual results to differ materially. Please refer to the special note regarding forward-looking statements in the company's quarterly report on Form 10-Q, which was filed today with the SEC and the Risk Factors section of the company's most recent annual report on Form 10-K for a discussion of these risks and uncertainties. Now I would like to turn the call over to Dr. Greg Demopulos, Chairman and CEO of Omeros.

早上好，感謝您今天加入通話。我想提醒您，今天的電話會議上發表的一些聲明將具有前瞻性。這些陳述僅基於管理層截至今天的信念和期望，並且可能會發生變化。所有前瞻性陳述均涉及風險和不確定性，可能導致公司的實際結果出現重大差異。請參閱今天向 SEC 提交的公司 10-Q 表格季度報告中關於前瞻性陳述的特別說明以及公司最新 10-K 表格年度報告的風險因素部分，以討論以下內容：這些風險和不確定性。現在我想將電話轉給 Omeros 董事長兼首席執行官 Greg Demopulos 博士。

Thank you, Jennifer, and good morning, everyone. Joining me here are Mike Jacobsen, Nadia Dac and Cathy Melfi, our respective heads of finance, commercial and regulatory. We'll start today with a brief overview of our financial results for the second quarter, followed by a corporate update. Mike will then provide a more detailed financial summary before we open the call to questions. Now let's look at our financial results.

謝謝你，詹妮弗，大家早上好。與我一起出席的還有我們各自的財務、商業和監管主管 Mike Jacobsen、Nadia Dac 和 Cathy Melfi。今天我們將首先簡要概述第二季度的財務業績，然後介紹公司最新情況。然後，在我們開始提問之前，邁克將提供更詳細的財務摘要。現在讓我們看看我們的財務業績。

Our GAAP net loss for the second quarter of 2023 was $37.3 million or $0.59 per share compared to a net loss of $33.7 million or $0.54 per share in the first quarter of this year. The increase was primarily due to research and development costs.

2023 年第二季度的 GAAP 淨虧損為 3730 萬美元，即每股 0.59 美元，而今年第一季度的淨虧損為 3370 萬美元，即每股 0.54 美元。增加的主要原因是研發成本。

Cash burn for the second quarter of 2023 was $30.1 million, which, as Mike will explain later, includes an artificial accounting-driven component of $3.4 million. OMIDRIA royalties for the second quarter were $10.7 million, a $1.5 million increase over first quarter royalties. As of June 30, 2023, to support ongoing operations and debt service, we had $341.3 million of cash and investments on hand and an additional $11.2 million in receivables, primarily consisting of OMIDRIA royalties.

2023 年第二季度的現金消耗為 3010 萬美元，其中包括 340 萬美元的人為會計驅動部分，邁克稍後將對此進行解釋。 OMIDRIA 第二季度特許權使用費為 1070 萬美元，比第一季度特許權使用費增加 150 萬美元。截至 2023 年 6 月 30 日，為了支持持續運營和償債，我們手頭有 3.413 億美元的現金和投資，以及另外 1120 萬美元的應收賬款，主要包括 OMIDRIA 特許權使用費。

Omeros has $95 million of convertible debt maturing in November. Our available cash and investments enable us to pay off these notes at maturity while continuing to fund operations and advancing our multiple programs well into 2025. As mandated by congressional legislation late last year, OMIDRIA secured separate payment from CMS and ambulatory surgery centers until at least January 2028. The legislation further mandates that beginning no later than January 2025, CMS will also pay separately for OMIDRIA when used in hospital outpatient departments.

Omeros 擁有 9500 萬美元的可轉換債務，將於 11 月到期。我們可用的現金和投資使我們能夠在到期時償還這些票據，同時繼續為運營提供資金並將我們的多個項目推進到2025 年。根據去年年底國會立法的規定，OMIDRIA 獲得了CMS 和門診手術中心的單獨付款，直到至少2028 年 1 月。立法進一步規定，不遲於 2025 年 1 月開始，CMS 還將單獨支付在醫院門診部使用 OMIDRIA 的費用。

Last month, CMS issued its proposed 2024 rule for the outpatient prospective payment system and consistent with the legislation called for ongoing separate payment of OMIDRIA. Let's turn now to our program update, starting first with our family of agents targeting MASP-2, the effector enzyme of the lectin pathway of complement. Narsoplimab is our lead antibody against MASP-2, our biologics license application or BLA for narsoplimab in hematopoietic stem cell transplant-associated thrombotic microangiopathy, or TA-TMA is pending with FDA. Following a recent meeting with FDA at which the agency reiterated its commitment to work with Omeros for the submission and provided helpful guidance on our proposal to collect and analyze external survival data.

上個月，CMS 發布了關於門診預期支付系統的 2024 年擬議規則，並與要求持續單獨支付 OMIDRIA 的立法相一致。現在讓我們來看看我們的程序更新，首先從我們針對 MASP-2（補體凝集素途徑的效應酶）的藥物家族開始。 Narsoplimab 是我們針對 MASP-2 的主要抗體，我們的 narsoplimab 治療造血幹細胞移植相關血栓性微血管病的生物製劑許可申請或 BLA 或 TA-TMA 正在向 FDA 申請。在最近與 FDA 舉行的會議上，該機構重申了與 Omeros 合作提交申請的承諾，並為我們收集和分析外部生存數據的提議提供了有用的指導。

We expect to submit to FDA early next month, a detailed plan of how we intend to analyze those survival data from already identified external sources. This proposal will be submitted as a Type B meeting request with FDA's response expected within 60 days. After receiving FDA's feedback on our detailed plan, we intend to conduct the analysis and together with additional new supportive data, plan to resubmit the BLA.

我們預計下月初向 FDA 提交一份詳細計劃，說明我們打算如何分析來自已確定的外部來源的生存數據。該提案將作為 B 類會議請求提交，FDA 預計將在 60 天內做出答复。在收到 FDA 對我們詳細計劃的反饋後，我們打算進行分析，並結合其他新的支持數據，計劃重新提交 BLA。

Assuming the full duration of relevant FDA review periods, we're targeting an approval decision by FDA in mid-2024. We'll update you when we have resubmitted the BLA. We continue to make narsoplimab available to both pediatric and adult patients worldwide under our expanded access or compassionate use program.

假設 FDA 相關審查期已滿，我們的目標是 FDA 在 2024 年中期做出批准決定。當我們重新提交 BLA 後，我們會通知您最新情況。根據我們的擴大使用或同情使用計劃，我們繼續向全世界的兒科和成人患者提供 narsoplimab。

To date, we've treated more than 125 compassionate use patients. Interestingly, a good number of patients have responded to narsoplimab despite failing treatment with eculizumab, ravulizumab and/or defibrotide. TA-TMA patients treated with narsoplimab under compassionate use have been the subject of numerous presentations by investigators at International Congresses.

迄今為止，我們已經治療了超過 125 名同情使用患者。有趣的是，儘管依庫珠單抗、拉維珠單抗和/或去纖苷治療失敗，但仍有大量患者對納索普利瑪有反應。在同情使用下接受 narsoplimab 治療的 TA-TMA 患者一直是研究人員在國際大會上進行的眾多演講的主題。

Most recently, a group of investigators in Italy submitted an abstract to the Annual Meeting of the American Society of Hematology, detailing the clinical and survival benefits of narsoplimab in 15 adult and pediatric compassionate use patients with severe TA-TMA. I'll turn now to our Phase III clinical program evaluating narsoplimab and IgA nephropathy. We remain on track to read out 36-week proteinuria data from our Phase III ARTEMIS-IGAN trial later this quarter.

最近，意大利的一組研究人員向美國血液學會年會提交了一份摘要，詳細介紹了 narsoplimab 在 15 名成人和兒童同情使用的嚴重 TA-TMA 患者中的臨床和生存獲益。我現在將談談我們評估 narsoplimab 和 IgA 腎病的 III 期臨床計劃。我們仍有望在本季度晚些時候讀出 III 期 ARTEMIS-IGAN 試驗的 36 週蛋白尿數據。

Despite the recent market entry of a steroid and a blood pressure medication, significant unmet need persists in IgA nephropathy. The lectin pathway of complement is increasingly recognized as a key immunologic driver of kidney injury and IgA nephropathy. A review article authored by an international group of experts and published in the most recent issue of Kidney International describes kidney biopsies from IgA nephropathy patients. These biopsies consistently showed glomerular deposition of mannan-binding lectin or MBL, together with IgA1 and up to 50% of patients with IgA nephropathy.

儘管類固醇和降血壓藥物最近進入市場，但 IgA 腎病的需求仍然存在嚴重未滿足的情況。補體凝集素途徑越來越被認為是腎損傷和 IgA 腎病的關鍵免疫驅動因素。由國際專家組撰寫並發表在最新一期《Kidney International》上的評論文章描述了 IgA 腎病患者的腎活檢。這些活檢一致顯示甘露聚醣結合凝集素或 MBL 以及 IgA1 沉積在腎小球內，且 IgA 腎病患者的腎小球沉積率高達 50%。

Glomerular deposition of lectin pathway pattern recognition molecules like MBL is known to be associated with more severe glomerular damage as well as more severe proteinuria and hematuria, all of this meaning more severe IgA nephropathy. Studies also show that the lectin pathway contributes to tubulointerstitial fibrosis and IgA nephropathy. The lectin pathway is the only complement pathway linked to tubulointerstitial damage, which is thought to be the common road to a wide range of end-stage kidney diseases, not just IgA nephropathy. The primary endpoint in our Phase III ARTEMIS-IGAN trial is reduction in proteinuria at 36 weeks and a population of patients at high risk for progressive worsening to end-stage renal disease and dialysis, meaning those patients with baseline proteinuria greater than 2 grams per day. These high proteinuria patients represent about 50% to 60% of all IgA patients globally. And to our knowledge, narsoplimab is the only drug being evaluated in this specific population.

已知凝集素途徑模式識別分子（如 MBL）在腎小球沉積與更嚴重的腎小球損傷以及更嚴重的蛋白尿和血尿有關，所有這些都意味著更嚴重的 IgA 腎病。研究還表明，凝集素途徑會導致腎小管間質纖維化和 IgA 腎病。凝集素途徑是唯一與腎小管間質損傷相關的補體途徑，這被認為是導致多種終末期腎臟疾病的常見途徑，而不僅僅是 IgA 腎病。我們的III 期ARTEMIS-IGAN 試驗的主要終點是36 週時蛋白尿的減少，以及患有進行性惡化至終末期腎病和透析的高風險患者群體，這意味著那些基線蛋白尿每天大於2 克的患者。這些高蛋白尿患者約佔全球所有 IgA 患者的 50% 至 60%。據我們所知，narsoplimab 是唯一在這一特定人群中進行評估的藥物。

Underscoring the importance of proteinuria reduction and our focus on high proteinuria patients a poster presented by international experts at the 60th Congress of the European Renal Association in June, described an analysis of data from IgAN patients along with quality of life measures, associated with kidney disease. The study showed that higher urine protein excretion was associated with higher symptom burden and worse quality of life overall.

6 月，國際專家在歐洲腎臟協會第60 屆大會上展示了一張海報，強調了減少蛋白尿的重要性以及我們對高蛋白尿患者的關注，其中描述了對IgAN 患者數據的分析以及與腎臟疾病相關的生活質量指標。研究表明，較高的尿蛋白排泄量與較高的症狀負擔和較差的整體生活質量相關。

ARTEMIS-IGAN is a double-blind placebo-controlled trial assuming positive data. We will submit both a BLA in the U.S. and a marketing authorization application or MAA in Europe. IgA nephropathy is a multibillion dollar market opportunity worldwide, and there is no approved complement inhibitor for this disease.

ARTEMIS-IGAN 是一項雙盲安慰劑對照試驗，假設數據呈陽性。我們將在美國提交 BLA，在歐洲提交營銷授權申請或 MAA。 IgA 腎病在全球範圍內是一個價值數十億美元的市場機會，但目前還沒有批准用於治療這種疾病的補體抑製劑。

Our other narsoplimab Phase III program in an atypical hemolytic uremic syndrome remains a low priority as we have noted previously. Turning to narsoplimab in COVID-19 in acute respiratory distress syndrome or ARDS. Our work continues at the Omeros labs at the University of Cambridge. In patients with acute severe and long COVID-19, we have been collaborating with multiple U.K. consortium. We expect a number of important publications from this work. In addition, a manuscript detailing the beneficial effects of MASP-2 inhibition on both symptoms and survival, in chemically induced ARDS was published at the end of May in Frontiers and immunology. Another manuscript has been submitted for publication describing the pulmonary and central nervous system benefits of MASP-2 blockade on symptoms and survival in well-established animals of COVID-19 ARDS.

正如我們之前指出的，我們針對非典型溶血性尿毒症綜合徵的其他 narsoplimab III 期項目仍然處於低優先級。轉向 narsoplimab 治療 COVID-19 急性呼吸窘迫綜合徵或 ARDS。我們的工作在劍橋大學的 Omeros 實驗室繼續進行。對於急性、嚴重和長期的 COVID-19 患者，我們一直在與多個英國聯盟合作。我們期待這項工作能發表一些重要的出版物。此外，5 月底在《前沿與免疫學》雜誌上發表了一篇手稿，詳細介紹了 MASP-2 抑制對化學誘導的 ARDS 的症狀和生存的有益影響。另一份手稿已提交出版，描述了 MASP-2 阻斷對已確診的 COVID-19 ARDS 動物的症狀和生存的肺和中樞神經系統的益處。

Animal studies evaluating a MASP-2 inhibitor in H1N1 driven ARDS are now underway. Discussions are ongoing with BARDA, which has declared its interest in helping to develop agents to treat both COVID and ARDS. Following behind narsoplimab in the clinic is our next-generation long-acting MASP-2 inhibitor, OMS1029 designed to be complementary to narsoplimab. Data from our successfully completed Phase I single ascending dose clinical trial support both subcutaneous and intravenous dosing just once quarterly.

評估 MASP-2 抑製劑治療 H1N1 引發的 ARDS 的動物研究正在進行中。與 BARDA 的討論正在進行中，BARDA 已宣布有興趣幫助開發治療新冠肺炎和急性呼吸窘迫綜合徵的藥物。繼 narsoplimab 進入臨床後，我們的下一代長效 MASP-2 抑製劑 OMS1029 旨在與 narsoplimab 互補。我們成功完成的 I 期單劑量遞增臨床試驗的數據支持每季度一次皮下和靜脈給藥。

So very well suited for chronic use. Dosing in the multiple ascending dose study of OMS1029 in healthy subjects began last month and a Phase II program is slated to begin next summer. We've also made good progress in our orally administered MASP-2 inhibitor program together with intravenous narsoplimab and our long-acting subcutaneous inhibitor, OMS1029. We expect our oral MASP-2 blocker to complete a franchise of antibody and small molecule MASP-2 inhibitors, enabling Omeros to control first-line therapy for lectin pathway related diseases. And Omeros' complement franchise just continues to expand and strengthen. Our lead antibody targeting MASP-3, the key activator of the alternative pathway of complement continues to prove its prominence as an alternative pathway inhibitor.

因此非常適合長期使用。 OMS1029 在健康受試者中的多次遞增劑量研究於上個月開始，II 期項目預計於明年夏天開始。我們的口服 MASP-2 抑製劑項目以及靜脈注射 narsoplimab 和我們的長效皮下抑製劑 OMS1029 也取得了良好進展。我們預計我們的口服 MASP-2 阻滯劑將完善抗體和小分子 MASP-2 抑製劑的系列產品，使 Omeros 能夠控制凝集素途徑相關疾病的一線治療。 Omeros 的補充特許經營權還在繼續擴大和加強。我們針對 MASP-3（補體旁路途徑的關鍵激活劑）的先導抗體繼續證明其作為旁路途徑抑製劑的突出地位。

We're currently advancing OMS906 across 3 clinical trials designed to build rapidly on the clinical efficacy data already in hand for OMS906. Two of these trials are evaluating OMS906 for the treatment of paroxysmal nocturnal hemoglobinuria or PNH. The first is evaluating OMS906 and PNH patients who have not previously been treated with a complement inhibitor. The second trial has a switchover design, enrolling PNH patients receiving the C5 inhibitor ravulizumab, adding OMS906 to provide combination therapy with ravulizumab for 24 weeks and then providing OMS906 monotherapy in patients who demonstrate a hemoglobin response with the combination therapy.

我們目前正在通過 3 項臨床試驗推進 OMS906，旨在快速建立 OMS906 現有臨床療效數據。其中兩項試驗正在評估 OMS906 治療陣發性睡眠性血紅蛋白尿症或 PNH 的效果。第一個是評估先前未接受過補體抑製劑治療的 OMS906 和 PNH 患者。第二項試驗採用轉換設計，招募接受 C5 抑製劑 ravulizumab 的 PNH 患者，添加 OMS906 與 ravulizumab 聯合治療 24 週，然後對聯合治療表現出血紅蛋白反應的患者提供 OMS906 單藥治療。

The third OMS906 clinical program is underway in patients with complement 3 glomerulopathy or C3G, a rare kidney disease. We are amending the dose in this trial due to information already learned in the PNH program. In June, data from a prespecified interim analysis and our ongoing trial of OMS906 in treatment-naive PNH patients were presented at a late-breaker session of the 2023 Congress of the European Hematology Association or EHA. The presentation identified by EHA's Scientific Program committee as one of the top 5 late-breaking submissions and delivered in a special oral session is available on the Investor Relations page of our website.

第三個 OMS906 臨床項目正在針對補體 3 腎小球病或 C3G（一種罕見的腎臟疾病）患者進行。根據 PNH 計劃中已獲悉的信息，我們正在修改本次試驗的劑量。 6 月，在 2023 年歐洲血液學協會 (EHA) 大會的最後會議上公佈了預先指定的中期分析數據以及我們正在進行的 OMS906 在初治 PNH 患者中的試驗數據。該演示文稿被 EHA 科學計劃委員會認定為最新提交的 5 篇論文之一，並在特別口頭會議上發表，可在我們網站的投資者關係頁面上查看。

OMS906 is the only drug that has been reported to be able to restore gender normal hemoglobin levels in PNH patients, gender normal, meaning hemoglobin levels that based on gender are normal for women and men, respectively. This is important because normal hemoglobin levels are meaningfully higher in men than in women. Other drug companies in the PNH space have been using the lower limit of normal for women as the threshold for normal hemoglobin for all patients. Yet this level is substantially below the normal level for men. OMS906 has restored not just women, but also men to truly normal gender-specific hemoglobin levels.

OMS906是據報導唯一能夠恢復PNH患者性別正常血紅蛋白水平的藥物，性別正常，這意味著基於性別的血紅蛋白水平對於女性和男性分別是正常的。這很重要，因為男性的正常血紅蛋白水平明顯高於女性。 PNH 領域的其他製藥公司一直使用女性正常血紅蛋白下限作為所有患者正常血紅蛋白的閾值。然而這個水平大大低於男性的正常水平。 OMS906 不僅使女性，而且使男性恢復到真正正常的性別特異性血紅蛋白水平。

The trial evaluating OMS906 in treatment-naive patients is over enrolled and patient treatment and data collection are ongoing. Although enrollment has been completed, we have been informed by investigators that additional patients are requesting participation. We are evaluating a protocol amendment that could increase enrollment, but not delay study completion.

在初治患者中評估 OMS906 的試驗已超額入組，患者治療和數據收集正在進行中。儘管登記已經完成，但研究人員告知我們，還有更多患者請求參與。我們正在評估一項方案修正案，該修正案可以增加入學率，但不會延遲研究完成。

At the end of July, we performed another analysis of the data in hand. The results are robust and impressive and we plan to present them at the upcoming Congress of the American Society of Hematology in December. The second PNH trial, the switchover trial, has already been amended to a Phase II study and the first low-dose cohort has been enrolled. At study entry, these patients had all received ravulizumab but had an inadequate response with hemoglobin levels remaining below 10.5 grams per deciliter.

7月底，我們對手頭的數據進行了另一次分析。結果強勁且令人印象深刻，我們計劃在 12 月即將召開的美國血液學會大會上展示它們。第二項 PNH 試驗（轉換試驗）已修改為 II 期研究，並且第一個低劑量隊列已入組。在研究開始時，這些患者均接受了 ravulizumab，但反應不充分，血紅蛋白水平仍低於 10.5 克/分升。

We're targeting 12 patients in this study and already have dosed 7 with others in screening. These patients are receiving combination therapy of ravulizumab and OMS906 and the first will begin receiving OMS906 monotherapy shortly. We anticipate providing data on this cohort late this year or early next. It's important to remember that all OMS906 data already made public result from the lowest dose of OMS906 that we plan to evaluate in this program. And we are now moving to higher doses and exposures to allow for a longer dosing interval. Yet even at this lowest dose, our hemoglobin and LDH results compare very favorably to the detailed and publicly available data on other alternative pathway inhibitors on the market or in development.

我們在這項研究中針對 12 名患者，並且已經對其他 7 名患者進行了篩查。這些患者正在接受 ravulizumab 和 OMS906 的聯合治療，第一批患者將很快開始接受 OMS906 單藥治療。我們預計在今年年底或明年初提供有關該群體的數據。重要的是要記住，所有 OMS906 數據已經公開，結果來自我們計劃在此計劃中評估的最低劑量的 OMS906。我們現在正在轉向更高的劑量和暴露，以允許更長的給藥間隔。然而，即使在這個最低劑量下，我們的血紅蛋白和 LDH 結果與市場上或正在開發的其他替代途徑抑製劑的詳細和公開數據相比也非常有利。

This comparison is even more impressive, given that of the 10 OMS906 treated patients publicly reported in addition to the hemolytic anemia or red blood cell destruction caused by PNH. Two patients also have a plastic anemia and 2 others have myelodysplastic syndrome, both of which suppress bone marrow production of mature red blood cells. Despite not having formal diagnosis, other patients in the trial beyond these 4 also had evidence of bone marrow failure at study entry. Those other patients similarly have shown a strong response to OMS906 treatment. The OMS906 data to date underscore the potential of OMS906 as a premier therapy for PNH but beyond that, they also demonstrate the expected utility of OMS906 across a broad range of diseases and disorders involving the alternative pathway.

鑑於公開報導的 10 名 OMS906 治療患者除了 PNH 引起的溶血性貧血或紅細胞破壞之外，這種比較更令人印象深刻。兩名患者還患有塑性貧血，另外兩名患者患有骨髓增生異常綜合徵，這兩種疾病都會抑制骨髓產生成熟紅細胞。儘管沒有正式診斷，但除這 4 名患者外，試驗中的其他患者在進入研究時也有骨髓衰竭的證據。其他患者同樣對 OMS906 治療表現出強烈的反應。迄今為止的 OMS906 數據強調了 OMS906 作為 PNH 主要療法的潛力，但除此之外，它們還證明了 OMS906 在涉及替代途徑的廣泛疾病和病症中的預期效用。

Clinical data have demonstrated that OMS906 not only inhibits MASP-3 but that MASP-3 inhibition provides a marked level of alternative pathway suppression sufficient to inhibit complement-driven hemolysis in PNH, a high bar for efficacy. Given that our competitors in the field have already validated the alternative pathway inhibition is effective in multiple other diseases and disorders. Our data in PNH provide us with good reason to expect that MASP-3 inhibition with OMS906 will also be effective across these other indications. So how do we expect to differentiate OMS906 from its potential competitors? Well, both the target MASP-3 in the drug, OMS906 have multiple expected advantages over other alternative pathway targets and drugs already on the market or in development.

臨床數據表明，OMS906 不僅抑制 MASP-3，而且 MASP-3 抑制提供了顯著水平的替代途徑抑制，足以抑制 PNH 中補體驅動的溶血，這是療效的高標準。鑑於我們在該領域的競爭對手已經驗證了替代途徑抑制對於多種其他疾病和病症是有效的。 PNH 中的數據讓我們有充分的理由預期 OMS906 抑制 MASP-3 也將在這些其他適應症中有效。那麼我們如何才能將 OMS906 與其潛在競爭對手區分開來呢？嗯，OMS906 藥物中的靶點 MASP-3 比其他替代途徑靶點和已上市或正在開發的藥物具有多種預期優勢。

First, MASP-3 blockers do not inhibit the infection-fighting function of the classical pathway. By contrast, both C3 and C5 inhibitors block the classical pathways adaptive immune response and increased infection risk.

首先，MASP-3 阻滯劑不會抑制經典途徑的抗感染功能。相比之下，C3 和 C5 抑製劑都會阻斷經典途徑適應性免疫反應並增加感染風險。

Second, MASP-3 is known not to be an acute phase reactant and has very low native circulating levels relative to other alternative pathway targets. This should allow OMS906 to maintain inhibition of MASP-3 allowing more effective blockade of alternative pathway activation.

其次，已知 MASP-3 不是急性期反應物，並且相對於其他替代途徑靶標而言，其天然循環水平非常低。這應該允許 OMS906 維持對 MASP-3 的抑制，從而更有效地阻斷旁路途徑的激活。

Importantly, it's expected that these MASP-3 characteristics will translate to a substantially lower risk of breakthrough of the underlying disease with inhibition of MASP-3 than with C3, C5 and Factor B, all of which are acute phase reactants whose concentrations increase in the setting of inflammation such as infection or any other inflammatory condition.

重要的是，與 C3、C5 和因子 B 相比，預計這些 MASP-3 特性將轉化為通過抑制 MASP-3 來顯著降低潛在疾病突破的風險，所有這些都是急性期反應物，其濃度在炎症的情況，例如感染或任何其他炎症狀況。

When these increased target concentrations occur, they can exceed the inhibitory capability of the respective drugs dosing, leaving patients less protected from their life-threatening disease. The third important advantage is better patient convenience and compliance. We expect that MASP-3's favorable target characteristics together with the pharmacokinetics and pharmacodynamics of OMS906 will allow once quarterly subcutaneous and intravenous administration of our drug. These are expected to enhance patient convenience and compliance compared to other alternative pathway inhibitors on the market or in development.

當目標濃度增​​加時，它們可能會超過相應藥物劑量的抑制能力，從而使患者對危及生命的疾病的保護較差。第三個重要優勢是更好的患者便利性和依從性。我們預計 MASP-3 的有利靶標特性以及 OMS906 的藥代動力學和藥效學將允許我們的藥物每季度皮下和靜脈注射一次。與市場上或正在開發的其他替代途徑抑製劑相比，這些藥物預計將提高患者的便利性和依從性。

Based on our substantial data in hand and the significant expected advantages of our MASP-3 target and drug, our objective is to make OMS906, the first line standard of care for the treatment of PNH and a large number of other alternative pathway diseases and disorders. Okay. Let's now move on to OMS527, our PDE7 inhibitor program. We've shown and/or published that PDE7 inhibition in animal models blocks both craving and relapse across multiple substances of abuse, including opioids, cocaine, nicotine, and alcohol. PDE7 inhibition has also been shown in animals to be effective in treating compulsive disorders, specifically (inaudible) .

基於我們現有的大量數據以及我們的 MASP-3 靶點和藥物的顯著預期優勢，我們的目標是使 OMS906 成為治療 PNH 和大量其他替代途徑疾病和病症的一線護理標準。好的。現在讓我們繼續討論 OMS527，我們的 PDE7 抑製劑項目。我們已經證明和/或發表了在動物模型中抑制 PDE7 可以阻止對多種濫用藥物的渴望和復發，包括阿片類藥物、可卡因、尼古丁和酒精。 PDE7 抑制也在動物身上被證明可以有效治療強迫症，特別是（聽不清）。

Current anti-addiction agents depress the reward system, significantly diminishing enjoyment of other aspects of a patient's life, while having only a limited effect on craving. In contrast, PDE7 inhibitors block craving and relapse and importantly, do not appear to depress the reward system. So patients treated with our PDE7 inhibitors would be expected to avoid the negative effects on life enjoyment seen with other anti-addiction drugs. OMS527 treated patients would simply lose their craving for the substance of abuse or for the compulsion.

目前的抗成癮藥物會抑制獎賞系統，顯著降低患者生活其他方面的享受，同時對渴望的影響有限。相比之下，PDE7 抑製劑可以阻止渴望和復發，而且重要的是，它似乎不會抑制獎勵系統。因此，使用我們的 PDE7 抑製劑治療的患者有望避免其他抗成癮藥物對生活享受的負面影響。接受 OMS527 治療的患者只會失去對濫用物質或強迫行為的渴望。

Now with funding support from the National Institute on Drug Abuse, we are moving ahead at NIDA's request and in collaboration with them to develop our lead orally administered PDE7 inhibitor to treat cocaine use disorder.

現在，在國家藥物濫用研究所的資金支持下，我們正在應 NIDA 的要求並與他們合作開發我們的主要口服 PDE7 抑製劑，用於治療可卡因使用障礙。

The 3-year $6.7 million grant from NIDA is intended to support both preclinical and clinical work, including a randomized double-blind inpatient study comparing the safety and effectiveness of our PDE7 inhibitor to placebo in the treatment of adults with cocaine use disorder who received concurrent intravenous cocaine. Omeros also controls broad patents surrounding PDE7 inhibition and movement disorders. With our collaborators at Emory University, we are evaluating OMS527 as a potential treatment for levodopa-induced dyskinesias or LID. LID manifests as crippling involuntary movements in Parkinson's patients caused primarily by prolonged treatment with levodopa. Levodopa though, is the most widely prescribed and most effective drug used to treat Parkinson's disease. As a result, LID represents a large unmet patient need and a large market opportunity.

NIDA 提供的3 年期670 萬美元撥款旨在支持臨床前和臨床工作，包括一項隨機雙盲住院患者研究，比較我們的PDE7 抑製劑與安慰劑在治療同時接受可卡因使用障礙的成人患者中的安全性和有效性。靜脈注射可卡因。 Omeros 還控制著有關 PDE7 抑制和運動障礙的廣泛專利。我們與埃默里大學的合作者正在評估 OMS527 作為左旋多巴引起的運動障礙或 LID 的潛在治療方法。 LID 表現為帕金森病患者的嚴重不自主運動，主要是由長期左旋多巴治療引起的。然而，左旋多巴是治療帕金森病最廣泛使用和最有效的藥物。因此，LID 代表著大量未滿足的患者需求和巨大的市場機會。

More than 10 million patients are living with Parkinson's worldwide and reportedly 50% or more of those with at least 5 years of levodopa treatment suffer from LID. If treated long enough with levodopa, it's thought that effectively all Parkinson's patients will develop LID.

全球有超過 1000 萬帕金森病患者，據報導，在接受至少 5 年左旋多巴治療的患者中，50% 或更多患有 LID。如果左旋多巴治療時間足夠長，那麼實際上所有帕金森病患者都會患上 LID。

Only one drug extended-release amantadine is approved for the treatment of LID. In addition to its only marginal efficacy amantadine is fraught with multiple significant adverse side effects, a more effective and safer treatment is needed.

只有一種藥物緩釋金剛烷胺被批准用於治療 LID。除了其僅有的邊際療效外，金剛烷胺還存在多種顯著的不良副作用，因此需要更有效和更安全的治療方法。

Our collaborators in Emory have developed a primate model of LID, which is highly predictive of clinical efficacy. Extended release of amantadine has been evaluated in the Emory model. The Emory investigators have also used this model to assess OMS527 in LID. We're evaluating the data and we'll file patent applications as appropriate. We'll wrap up today's corporate review with our immuno-oncology programs. There are two broad arms of our IO franchise, our cellular platforms and our molecular platforms. In our two cellular platforms, we have developed novel approaches to both adoptive T-cell therapy and chimeric antigen receptor or CAR T-cell therapy. Both of these proprietary platforms are based on the novel identification of specific T-cell signaling pathways, which once inhibited significantly and preferentially potentiate and enhance the expansion of tumor-specific memory T-cells that distinctively recognize and efficiently kill tumor cells.

我們在埃默里大學的合作者開發了一種靈長類動物 LID 模型，該模型可以高度預測臨床療效。金剛烷胺的緩釋已在埃默里模型中進行了評估。埃默里大學的研究人員還使用該模型來評估 OMS527 在 LID 中的作用。我們正在評估數據，並將酌情提交專利申請。我們將通過我們的免疫腫瘤學項目來結束今天的企業審查。我們的 IO 專營權有兩大領域：細胞平台和分子平台。在我們的兩個細胞平台中，我們開發了過繼性 T 細胞療法和嵌合抗原受體或 CAR T 細胞療法的新方法。這兩個專有平台均基於對特定T 細胞信號通路的新穎識別，該通路一旦被顯著抑制，就會優先增強和增強腫瘤特異性記憶T 細胞的擴增，從而獨特地識別並有效殺死腫瘤細胞。

Our adoptive T-cell platform is designed to target both cell surface and intracellular cancer antigen significantly broadening its range of indications. Further, unlike existing CAR T therapies, our adoptive T cell technology does not require cellular modification or engineering. This represents a potentially major advance over currently available adoptive T cell therapies, markedly decreasing cost and the time required for treatment preparation while enhancing efficacy by enabling multiple repetitive administrations. The result we expect will be a better and sustained antitumor response.

我們的過繼性 T 細胞平台旨在針對細胞表面和細胞內癌症抗原，顯著拓寬其適應症範圍。此外，與現有的 CAR T 療法不同，我們的過繼性 T 細胞技術不需要細胞修改或工程。這代表著相對於目前可用的過繼性 T 細胞療法的潛在重大進步，顯著降低了治療準備所需的成本和時間，同時通過多次重複給藥來提高療效。我們期望的結果將是更好且持續的抗腫瘤反應。

Also in our modified CAR T technology, we've incorporated an immunomodulator of T cell signaling, which protects T cells from the immunosuppressive environment promoted by cancer cells. Another important benefit over existing CAR T therapies. Our CAR T modifications significantly potentiates the efficacy and sustained response of Omeros' CAR T therapy. Our team is validating these novel cellular adoptive T-cell and CAR-T platforms and is establishing a broad patent estate around them. We believe that these proprietary technologies could meaningfully and substantially improve response rates for cancer patients receiving either engineered or native T-cell therapies for not just liquid tumors like existing cellular therapies, but for both liquid and solid tumors.

此外，在我們改進的 CAR T 技術中，我們融入了 T 細胞信號傳導的免疫調節劑，可保護 T 細胞免受癌細胞促進的免疫抑制環境的影響。相對於現有 CAR T 療法的另一個重要優勢。我們的 CAR T 修飾顯著增強了 Omeros CAR T 療法的功效和持續反應。我們的團隊正在驗證這些新穎的細胞過繼 T 細胞和 CAR-T 平台，並圍繞它們建立廣泛的專利資產。我們相信，這些專有技術可以有意義且實質性地提高接受工程或天然 T 細胞療法的癌症患者的反應率，不僅針對現有細胞療法等液體腫瘤，而且針對液體腫瘤和實體瘤。

Our other IO platforms, our molecular therapy platforms, our biologics designed to be injected directly into the patient and include therapeutic cancer vaccines, immunomodulators and modified toxins or what we term our Oncotox platform. Successful development of therapeutic cancer vaccines will widely pursued remains difficult to achieve with the current approach is inducing only transient and ineffective immune responses.

我們的其他 IO 平台、我們的分子治療平台、我們設計用於直接注射到患者體內的生物製劑，包括治療性癌症疫苗、免疫調節劑和改良毒素，或者我們稱之為 Oncotox 平台。由於目前的方法只能誘導短暫且無效的免疫反應，因此要廣泛追求的治療性癌症疫苗的成功開發仍然很難實現。

We believe that we've discovered a way to overcome this challenge, having now generated novel molecules that combine tumor antigens with a potent adjuvant. These molecules activate antigen-presenting cells, which in turn lead to amplification of cancer-specific T and B cells. When injected into the body, these novel biologics should result in not only elimination of currently present tumor cells, but importantly, immune memory against future cancer relapse. Our immunomodulator platform is designed to target and activate immune cells to convert cold tumors into hot.

我們相信，我們已經找到了克服這一挑戰的方法，現在已經產生了將腫瘤抗原與有效佐劑結合起來的新型分子。這些分子激活抗原呈遞細胞，進而導致癌症特異性 T 細胞和 B 細胞擴增。當注射到體內時，這些新型生物製劑不僅可以消除當前存在的腫瘤細胞，而且重要的是，可以產生針對未來癌症復發的免疫記憶。我們的免疫調節劑平台旨在靶向和激活免疫細胞，將冷腫瘤轉化為熱腫瘤。

A cold tumor is one that is refractory to immune therapy because it's microenvironment suppresses the activation and function of therapeutic immune cells. Omeros's immunomodulators are designed to make the immune cells resistant to these suppressive conditions and restore the functionality of the therapeutic immune cells. As a consequence, lymphocytes, macrophages, antigen presenting and other immune cells can infiltrate the tumor, converting it from a cold to a hot tumor allowing the tumor to be destroyed.

冷腫瘤是一種免疫治療難治性腫瘤，因為它的微環境抑制了治療性免疫細胞的激活和功能。 Omeros 的免疫調節劑旨在使免疫細胞對這些抑制條件產生抵抗力，並恢復治療性免疫細胞的功能。因此，淋巴細胞、巨噬細胞、抗原呈遞細胞和其他免疫細胞可以浸潤腫瘤，將其從冷腫瘤轉變為熱腫瘤，從而使腫瘤被破壞。

Finally, our Oncotox platform uses engineered toxins to kill only cancer cells that are actively proliferating while not affecting organs or any healthy cells. We expect that this novel approach will avoid the deleterious side effects resulting from currently available toxin caring therapeutics especially damage to endothelial cells, vascular leak as well as serious complications, including death, have severely hindered the use of currently marketed toxins.

最後，我們的 Oncotox 平台使用工程毒素僅殺死活躍增殖的癌細胞，而不影響器官或任何健康細胞。我們期望這種新方法將避免目前可用的毒素治療療法產生的有害副作用，特別是對內皮細胞的損傷、血管滲漏以及包括死亡在內的嚴重並發症，這些都嚴重阻礙了目前市售毒素的使用。

We expect our Oncotox platform to have a significantly higher safety margin and broader applications than those currently marketed approaches. Based on the preclinical data generated to date, all three of our molecular platforms, namely cancer vaccines, immunomodulators and oncotox have the potential to be long-acting and to improve survival rates significantly across both solid and hematologic or liquid tumors.

我們預計我們的 Oncotox 平台將比目前市售的方法具有更高的安全裕度和更廣泛的應用。根據迄今為止產生的臨床前數據，我們的所有三個分子平台，即癌症疫苗、免疫調節劑和oncotox，都有可能具有長效作用，並顯著提高實體瘤和血液或液體腫瘤的生存率。

I'll now turn the call over to Mike Jacobsen, our Chief Accounting Officer to go through a more detailed discussion of our second quarter financial results. Mike?

現在，我將把電話轉給我們的首席會計官邁克·雅各布森 (Mike Jacobsen)，以更詳細地討論我們第二季度的財務業績。麥克風？

Yes. Thanks, Greg. Our net loss for the second quarter was $37.3 million or $0.59 per share compared to a net loss of $33.7 million or $0.54 per share in the first quarter of this year. Cash burn for the second quarter of 2023 was $30.1 million. Royalties are generally paid 60 days after the month they are earned. Although the $3.4 million payment due on June 30 was received on July 3.

是的。謝謝，格雷格。我們第二季度的淨虧損為 3730 萬美元，即每股 0.59 美元，而今年第一季度的淨虧損為 3370 萬美元，即每股 0.54 美元。 2023 年第二季度的現金消耗為 3010 萬美元。特許權使用費通常在賺取當月後 60 天支付。儘管 6 月 30 日到期的 340 萬美元付款已於 7 月 3 日收到。

This late payment artificially increased our second quarter cash burn by $3.4 million. As of June 30, 2023, we had $341 million of cash and investments on hand and $11 million in receivables, which primarily consists of the OMIDRIA royalties.

這次逾期付款人為地增加了我們第二季度的現金消耗 340 萬美元。截至 2023 年 6 月 30 日，我們手頭有 3.41 億美元的現金和投資，以及 1100 萬美元的應收賬款，其中主要包括 OMIDRIA 特許權使用費。

Costs and expenses from continuing operations for the second quarter was $40.9 million, an increase of $5.2 million from the first quarter of this year.

第二季度持續運營成本和費用為 4090 萬美元，比今年第一季度增加 520 萬美元。

The increase was primarily due to additional research and development costs related primarily to drug manufacturing and to clinical costs associated with our Phase III clinical trial of narsoplimab in IgA nephropathy as well as site start-up expenses for our 906 studies. Interest expense for the second quarter was $7.9 million, which was consistent with the first quarter of this year.

這一增長主要是由於主要與藥品生產相關的額外研發成本、與 narsoplimab 治療 IgA 腎病的 III 期臨床試驗相關的臨床成本以及我們 906 研究的現場啟動費用。第二季度利息支出為790萬美元，與今年第一季度持平。

The primary drivers of interest expense are the 2023 and 2026 unsecured convertible senior notes and the DRI OMIDRIA royalty obligation. Now let's look at OMIDRIA royalties. Under our current contract with the Rayner, OMIDRIA royalties decreased from 50% to 30% of U.S. net sales up on earning the $200 million milestone payment at the end of last year.

利息支出的主要驅動因素是 2023 年和 2026 年無擔保可轉換優先票據和 DRI OMIDRIA 特許權使用費義務。現在讓我們看看 OMIDRIA 版稅。根據我們與 Rayner 目前的合同，OMIDRIA 特許權使用費從美國淨銷售額的 50% 下降到去年底獲得 2 億美元里程碑付款的 30%。

While separate payment for OMIDRIA is in effect, the 30% royalty rate will apply throughout the duration of the relevant patent terms, which we expect to be at least through 2033. For the second quarter of 2023, our royalties on OMIDRIA net sales were $10.7 million. Royalties earned are recorded as a reduction in the OMIDRIA contract royalty asset on the balance sheet. Income from discontinued operations in the second quarter was $7 million, includes 2 primary components. $3.8 million of interest earned on the OMIDRIA contract royalty asset and $3.1 million of income due to remeasurement adjustments on our OMIDRIA contract royalty asset.

雖然對OMIDRIA 的單獨付款有效，但30% 的特許權使用費將適用於整個相關專利期限，我們預計至少會持續到2033 年。2023 年第二季度，我們對OMIDRIA 淨銷售額的特許權使用費為10.7 美元百萬。賺取的特許權使用費在資產負債表上記錄為 OMIDRIA 合同特許權使用費資產的減少。第二季度來自已終止業務的收入為 700 萬美元，包括 2 個主要組成部分。 OMIDRIA 合同特許權使用費資產賺取了 380 萬美元的利息，由於 OMIDRIA 合同特許權使用費資產的重新計量調整而獲得了 310 萬美元的收入。

Now let's take a minute and talk about expected third quarter results. We expect overall operating costs from continuing operations in the third quarter to increase by approximately $5 million to $6 million. The increase is primarily due to our planned payment of a $5 million milestone obligation tied to advancing clinical development in our OMS906 program and the timing of certain manufacturing activities.

現在讓我們花一點時間談談預期的第三季度業績。我們預計第三季度持續運營的總體運營成本將增加約 500 萬美元至 600 萬美元。這一增長主要是由於我們計劃支付 500 萬美元的里程碑義務，該義務與推進 OMS906 項目的臨床開發以及某些製造活動的時間安排有關。

Interest income in the third quarter should be nearly $4 million and interest expense for Q3 should be consistent with the second quarter at approximately $8 million. Income from discontinued operations for the third quarter should be approximately $6 million. With that, I'll turn the call back over to Greg. Greg?

第三季度的利息收入應接近 400 萬美元，第三季度的利息支出應與第二季度保持一致，約為 800 萬美元。第三季度來自已終止業務的收入應約為 600 萬美元。這樣，我會將電話轉回給格雷格。格雷格？

Thanks, Mike. Operator, let's open the call to questions.

謝謝，邁克。接線員，讓我們開始提問。

(Operator Instructions) Our first question comes from the line of Colin Bristow with UBS.

（操作員說明）我們的第一個問題來自 UBS 的 Colin Bristow 線路。

Thanks for all the helpful color here. First on narsoplimab in the TA-TMA. Can you give a little more color on what were the agencies' key concerns or points of focus in the May meeting? And then any detail on the specifics of the survival assets plan would also be helpful. And then just second, on the IgAN, what are you having to see in the proteinuria data and any of the components of this update that you would highlight at this stage?

感謝這裡所有有用的顏色。首先是 TA-TMA 中的 narsoplimab。您能否詳細說明一下各機構在 5 月份會議上的主要關切或焦點是什麼？然後，有關生存資產計劃細節的任何細節也會有所幫助。其次，在 IgAN 上，您在蛋白尿數據中需要看到什麼，以及您在這個階段要強調的本次更新的任何組成部分？

Sure. I think having -- we're having a little trouble hearing you here. But I think the first question was, are there any concerns or what if any, concerns does FDA have with respect to our BLA resubmission process. And I think that the answer to that would be, I don't think there are specific concerns. I think that FDA is wanting to make sure that the data we provide are robust that the data we provide demonstrate a survival benefit in the narsoplimab treated group versus the external control sources. So I think really, the onus is on us at Omeros to make sure that we satisfy all of those requests by FDA. So I'll look to Cathy, who is here and our Head of Regulatory, to add anything to that she'd like.

當然。我認為——我們在這裡聽到你的聲音有點困難。但我認為第一個問題是，FDA 對我們的 BLA 重新提交流程是否有任何擔憂或擔憂（如果有的話）。我認為答案是，我不認為有具體的擔憂。我認為 FDA 希望確保我們提供的數據是可靠的，我們提供的數據證明 narsoplimab 治療組與外部對照源相比具有生存獲益。所以我認為，Omeros 確實有責任確保滿足 FDA 的所有要求。因此，我將請 Cathy（我們的監管主管）補充她想要的內容。

Yes. And as Greg mentioned in the call, FDA have indicated that they're committed to working with us in terms of the resubmission of the BLA. And we believe the data that we have are will be strong and the approach consistent with the path forward that was presented to us. And so again, we're just continuing to work with FDA.

是的。正如 Greg 在電話中提到的，FDA 已表示他們致力於在重新提交 BLA 方面與我們合作。我們相信，我們擁有的數據將是強有力的，並且方法與向我們提出的前進道路一致。同樣，我們只是繼續與 FDA 合作。

Okay. And Colin, I'm sorry, really, I think everyone in the room sort of did not quite hear your second question. I know it was tied to IgAN but it sort of trailed off and we could not hear it here. Would you mind just repeating your second question?

好的。科林，我很抱歉，真的，我認為房間裡的每個人都沒有完全聽到你的第二個問題。我知道它與 IgAN 有關，但它有點減弱，我們在這裡聽不到它。您介意重複一下您的第二個問題嗎？

Just on the upcoming IgAN readout. I was just wondering what are you hoping to see in the proteinuria data, any specific thresholds? And any other components of the update that you would highlight to us or have a focus on.

就在即將到來的 IgAN 讀數上。我只是想知道您希望在蛋白尿數據中看到什麼，有什麼具體的閾值嗎？以及您向我們強調或關注的更新的任何其他組件。

Okay. No, thank you for repeating that. Understood. We don't have a specific threshold that we're targeting in IgAN. I mean, I think it's important to look at how other agents that have been approved have performed. And I think those numbers are ranging as a delta over placebo at around high 20s and I think that clearly indicates what is approvable. As you know, there is no approved complement inhibitor. So we really don't see our competitors as either a steroid or additional RAS blockade. I mean always in IgA patients you're going to want to optimize RAS blockade. And steroids, KDIGO has recommended when you can't -- when a clinician cannot get a handle on the IgA that a 6-month course of steroids is warranted, but that's really only 6 months.

好的。不，謝謝你重複一遍。明白了。我們沒有針對 IgAN 設定具體的閾值。我的意思是，我認為了解其他已獲批准的藥物的表現非常重要。我認為這些數字與安慰劑相比相差 20 左右，我認為這清楚地表明了哪些內容是可以批准的。如您所知，還沒有批准的補體抑製劑。因此，我們確實不認為我們的競爭對手是類固醇或額外的 RAS 封鎖劑。我的意思是，對於 IgA 患者，您始終需要優化 RAS 阻斷。至於類固醇，當臨床醫生無法掌握 IgA 時，KDIGO 會推薦您使用 6 個月的類固醇療程，但實際上只有 6 個月。

And the budesonide that has been approved has been approved really for only 1 9-month period. So we don't see either of those as competitors. What we need to do is see the data understand the data and go forward from there. I mean we expect the data to be positive. Of course, we can't guarantee that. But if we look at all the data we have generated with narsoplimab as well as the mechanism of action. As I said earlier, MASP-2 inhibition not only is important in the glomerulus, but also in the tubulointerstitial which is why in patients with long-standing IgA nephropathy patients whose disease in the glomerulus should have long ago burned out. We saw marked reduction in proteinuria and stabilization even improvement in some patients in eGFR.

而已經批准的布地奈德實際上只批准了1個9個月的期限。因此，我們不將其中任何一個視為競爭對手。我們需要做的是看到數據、理解數據並以此為基礎繼續前進。我的意思是我們預計數據會是積極的。當然，我們不能保證這一點。但是，如果我們查看使用 narsoplimab 生成的所有數據以及作用機制。正如我之前所說，MASP-2 抑制不僅在腎小球中很重要，而且在腎小管間質中也很重要，這就是為什麼對於長期患有IgA 腎病的患者，其腎小球疾病應該早就消失了。我們看到一些患者的蛋白尿明顯減少，eGFR 穩定甚至改善。

So as to the best of our knowledge, MASP-2 inhibition is the only mechanism that works at both those sites. So we're looking forward to the data. We look forward to sharing the data. I think with respect to the question is, is there anything else that we want to see. Look, we're looking specifically at high protein spillers, patients with 2 or more grams of proteinuria per day. We're doing that because that's of high interest to FDA. These are patients who rapidly and continue to progressively advance to end-stage renal disease and dialysis. We've selected that group for a specific reason, and as I've just laid out. So I think we're eager to see the data. We're eager to share the data. Once we have them in hand, we'll have a lot more to say.

據我們所知，MASP-2 抑制是在這兩個位點都起作用的唯一機制。所以我們很期待數據。我們期待分享數據。我認為問題是，還有什麼我們想看到的嗎？看，我們專門關注高蛋白溢出者，即每天蛋白尿量達到或超過 2 克的患者。我們這樣做是因為 FDA 對此非常感興趣。這些患者迅速並持續進展為終末期腎病並需要透析。正如我剛才所闡述的那樣，我們出於特定原因選擇了該小組。所以我認為我們渴望看到數據。我們渴望分享數據。一旦我們掌握了它們，我們就會有更多的話要說。

One moment for your next question, please. Our next question comes from the line of Steve Brozak with WBB Securities.

請稍等一下，回答你的下一個問題。我們的下一個問題來自 WBB 證券公司的 Steve Brozak。

One quick question and one housekeeping question, but let me go to the question. On the compassionate use that you mentioned early in the call, can you give us any details on what's taking place there and specifically around -- any changes, any increase, what the clinicians are telling you? Anything you can do to help that, obviously, specifically in the TA-TMA space, please?

一個簡單的問題和一個內務問題，但讓我直接回答這個問題。關於您在電話中早些時候提到的富有同情心的使用，您能否向我們提供有關那裡發生的情況的任何詳細信息，特別是周圍發生的情況- 任何變化，任何增加，臨床醫生告訴您什麼？顯然，您可以做些什麼來幫助實現這一目標，特別是在 TA-TMA 領域，好嗎？

Yes. Sure, Steve. Thanks. With respect to compassionate use in TA-TMA for narsoplimab, as I said, we have provided drug under compassionate use for over 125 patients. These are both adult and pediatric patients worldwide. We don't have full case report forms or case report forms really to speak up for these patients, given that it's an extended use or compassionate use program. But we do get feedback. And that feedback is also made public through the multiple presentations at International Congresses by the investigators who request and then use narsoplimab to treat their patients. It is, I think, notable that we receive multiple requests from the same institutions and this is not a small set of institutions, obviously, with 125-plus patients. But we -- across that 125-plus patient number, we're receiving repeated requests from institutions. And obviously, our conclusion from that is the drug must be doing something good. Otherwise, they would not be repeatedly requesting it for their patients, both adult and pediatric.

是的。當然，史蒂夫。謝謝。關於 TA-TMA 中 narsoplimab 的同情使用，正如我所說，我們已經為超過 125 名患者提供了同情使用的藥物。這些患者都是世界各地的成人和兒童患者。鑑於這是一項擴展使用或同情使用計劃，我們沒有完整的病例報告表或真正為這些患者說話的病例報告表。但我們確實得到了反饋。這些反饋也通過研究人員在國際大會上的多次演講公開，他們要求並使用 narsoplimab 來治療患者。我認為值得注意的是，我們收到了來自同一機構的多個請求，顯然，這不是一小部分機構，擁有 125 多名患者。但在 125 多名患者中，我們不斷收到來自各機構的請求。顯然，我們的結論是這種藥物一定有好處。否則，他們不會反复要求為成人和兒童患者提供這種服務。

As I mentioned in the prepared comments, interestingly also, we are seeing patients who have failed other therapies, C5 inhibitors, eculizumab, ravulizumab defibrotide as well, who are then treated with narsoplimab. So effectively, at that point, we're catching a falling knife. These are patients who are very, very sick, have gone for a while with the TA-TMA progressing, moving to end-stage organ failure or having organ failure. And yet we treat them because we do not want to deny these patients.

正如我在準備好的評論中提到的，有趣的是，我們看到其他療法、C5 抑製劑、依庫麗珠單抗、ravulizumab 去纖苷治療失敗的患者，然後接受 narsoplimab 治療。就這樣，我們有效地接住了一把掉落的刀。這些患者病情非常非常嚴重，已經經歷了一段時間的 TA-TMA 進展，進入終末期器官衰竭或患有器官衰竭。然而我們治療他們是因為我們不想拒絕這些患者。

We treat them and they recover. If you see that once you see that twice, you might say, (inaudible), that's just coincidence or an act of God. You see that enough times and I think it becomes pretty clear that the drug is effective. And the latter is what we're seeing. So let me see if that answers your question.

我們治療他們，他們就康復了。如果您看到這一點，一旦您看到兩次，您可能會說，（聽不清），這只是巧合或上帝的行為。你看的次數足夠多了，我想很明顯這種藥物是有效的。後者就是我們所看到的。那麼讓我看看這是否能回答您的問題。

No, thank you for the answer and obviously, these patients thank you for the answer and what you've done. So that is a succinct an explanation as you can ask for. On the housekeeping side, and then I'll jump back in the queue. Earlier in the call, you reiterated and I looked online, and you basically stated that the loss was $0.59, but I'm seeing some other places reporting a $0.70 loss I believe that's a typo, but I just want to make sure that you reiterate that number at $0.59 and there's no other issues around the -- what we're seeing elsewhere.

不，謝謝您的回答，顯然，這些患者感謝您的回答和您所做的事情。這是您可以要求的簡潔的解釋。在客房服務方面，然後我會插回隊列。在電話會議的早些時候，你重申了，我在網上查了一下，你基本上說損失是0.59 美元，但我看到其他一些地方報告了0.70 美元的損失，我認為這是一個錯字，但我只是想確保你重申這個數字為 0.59 美元，並且沒有其他問題——我們在其他地方看到的情況。

No, there's not. The $0.59 per share loss is the correct GAAP number. I think what is happening, and we've tried to correct this multiple times on our earnings calls. But I think what's happening is the $0.70 is being lifted from continuing operations. But we are required by accounting rules to account for our royalties in noncontinuing operations. So that whole piece is clearly being missed. I think when many report our EPS. So it's looking at just continuing operations, ignoring noncontinuing operations and within the noncontinuing operations are all of our royalties that we receive. But it's just -- it's a function of accounting and accounting requirements. Let me see if Mike, do you have anything to add to that or make that more clear.

不，沒有。每股虧損 0.59 美元是正確的 GAAP 數字。我認為正在發生的事情，我們已經在財報電話會議上多次嘗試糾正這一問題。但我認為正在發生的事情是 0.70 美元從持續運營中被取消。但會計規則要求我們對非持續經營業務中的特許權使用費進行核算。所以整個部分顯然被遺漏了。我認為當許多人報告我們的每股收益時。因此，它只關注持續經營業務，忽略非持續經營業務，非持續經營業務是我們收到的所有特許權使用費。但這只是——它是會計和會計要求的函數。讓我看看邁克，您是否還有什麼要補充的或者說得更清楚的。

Yes. I think the key to know is our discontinued operations is going to continue as long as we get OMIDRIA royalty. A lot of times, discontinued operations is a year or 2 when it's gone. But in our case, the way the accounting made us do this, we will continue to have discontinued operations. OMIDRIA royalties are obviously a significant positive cash flow for us and using discontinuing operations miss is a big part of our finance.

是的。我認為關鍵是要知道，只要我們獲得 OMIDRIA 特許權使用費，我們已停止的業務就會繼續下去。很多時候，停業一兩年後就消失了。但就我們而言，按照會計要求我們這樣做，我們將繼續停止運營。 OMIDRIA 特許權使用費對我們來說顯然是一筆重要的正現金流，而使用中止經營損失是我們財務的重要組成部分。

One moment for our next question, please and our next question comes from the line of Greg Harrison with Bank of America.

請稍等一下我們的下一個問題，我們的下一個問題來自美國銀行的格雷格·哈里森 (Greg Harrison)。

Is there any color you can provide about your latest interim analysis on OMS906, you mentioned in the press release and how consistent those results were with what you presented at EHA?

對於您在新聞稿中提到的對 OMS906 的最新中期分析，您是否可以提供任何信息，以及這些結果與您在 EHA 上展示的結果是否一致？

Sure. Thanks, Greg. We want to be careful here that we don't preempt what we have submitted for presentation at ASH. But I think we can speak to it in general terms. We are seeing very consistent results. And as we move further out in time, one might expect that we are seeing continued improvement. So we're very encouraged by what we're seeing. The latest cut of the data only reinforces, I think, our confidence in the target and our confidence in the drug. But again, not just in PNH, but more broadly across really a very wide range of alternative pathway-related diseases and disorders. PNH is a good litmus test because you really do need to effectively ablate alternative pathway activity and if you don't do that, you see it pretty quickly in your LDH levels and shortly thereafter in your hemoglobin levels.

當然。謝謝，格雷格。我們要小心，不要搶占我們在 ASH 上提交的演示內容。但我認為我們可以籠統地談論它。我們看到了非常一致的結果。隨著時間的推移，人們可能會期望我們看到持續的改進。因此，我們對所看到的感到非常鼓舞。我認為，最新的數據削減只會增強我們對目標和藥物的信心。但同樣，不僅在 PNH 中，而且更廣泛地涉及非常廣泛的替代途徑相關疾病和病症。 PNH 是一個很好的試金石，因為您確實需要有效地消除旁路途徑活性，如果您不這樣做，您很快就會在LDH 水平中看到它，隨後不久就會在血紅蛋白水平中看到它。

So it's a very good litmus test on how effective a drug is in inhibiting alternative pathway activation. And we're clearly seeing that OMS906 is highly effective. And then that should be translatable to the other alternative pathway indications. And really, with the other therapeutics in the space, it's pretty easy for us to identify what is an alternative pathway-related disease or disorder and what is not. And we can then follow those other agents and what will be with an agent that we expect has significant advantages as well as the target having significant advantages over other drugs and other targets. I'll see if Nadia, do you have any additional comments?

因此，這是一個非常好的試金石，可以檢驗藥物抑制旁路途徑激活的效果。我們清楚地看到 OMS906 非常有效。然後這應該可以轉化為其他替代途徑適應症。事實上，通過該領域的其他療法，我們很容易識別什麼是與替代途徑相關的疾病或紊亂，什麼不是。然後我們可以跟踪那些其他藥物，以及我們期望具有顯著優勢的藥物以及相對於其他藥物和其他目標具有顯著優勢的目標。我看看娜迪亞，你還有什麼意見嗎？

I think one of the things I'll add and not only for 906, but our portfolio is also the advantage of lessening treatment burden on these patients. And having patients taking daily pills or very often injections and things like that is another key differentiator. And so we're excited across the entire portfolio, including 906 for this additional advantage.

我認為我要補充的一件事不僅是針對 906，而且我們的產品組合還有減輕這些患者的治療負擔的優勢。讓患者每天服用藥物或經常注射或類似的東西是另一個關鍵的區別因素。因此，我們對整個產品組合感到興奮，包括 906 的這一額外優勢。

Thank you, Nadia. So as you see, I mean, we've got relatively short-acting IV. We have long-acting IV or subcu and now in MASP-2, we're moving pretty quickly on our oral. And that's looking good as well. So we have the landscape covered, and we control the effector enzyme of the lectin pathway, which effectively means we control the lectin pathway. And we also control the key activator of the alternative pathway with all of the advantages that Nadia just mentioned and that I went through in the prepared comments. So we really do believe that we can make a very strong case that we have the premier complement franchise in the industry full stop.

謝謝你，納迪亞。正如你所看到的，我的意思是，我們的靜脈注射作用相對較短。我們有長效 IV 或 subcu，現在在 MASP-2 中，我們在口服方面進展得相當快。這看起來也不錯。所以我們已經覆蓋了景觀，並且我們控制了凝集素途徑的效應酶，這實際上意味著我們控制了凝集素途徑。我們還控制了替代途徑的關鍵激活劑，具有納迪亞剛才提到的以及我在準備好的評論中經歷過的所有優勢。因此，我們確實相信我們可以強有力地證明我們擁有行業內首屈一指的補充特許經營權。

Next question comes from Serge Belanger with Needham.

下一個問題來自 Serge Belanger 和 Needham。

A couple on the IgAN program. Maybe can you talk about the statistical powering of the trial that's going to read out later this quarter? And secondly, do you believe the ARTEMIS trial is the only Phase III trial required to support BLA and MAA filing in Europe? And then my second question -- I guess, third question, regarding the nonpaying coverage in OMIDRIA. OMIDRIA had some good traction in the ASC setting. Just curious how the no paying coverage that takes effect in 2025 will change the overall coverage of the product and whether it will see increased usage beyond the ASC study?

一對參加 IgAN 計劃的夫婦。也許您能談談本季度晚些時候將公佈的試驗的統計功效嗎？其次，您是否認為 ARTEMIS 試驗是支持在歐洲提交 BLA 和 MAA 所需的唯一 III 期試驗？然後是我的第二個問題——我想是第三個問題，關於 OMIDRIA 的非付費保險。 OMIDRIA 在 ASC 環境中具有良好的吸引力。只是好奇 2025 年生效的免費覆蓋範圍將如何改變該產品的整體覆蓋範圍，以及除了 ASC 研究之外，該產品的使用量是否會增加？

Sure. Thanks, Serge. In answer to your first question, the IgAN powering, our statisticians believe that and are quite confident that we are overpowered. So I think we're in good shape there. And yes, we expect that the one Phase III clinical trial will be sufficient to support a BLA and MAA, and that's consistent with other therapeutics that have received approval recently. So we see no difference there.

當然。謝謝，塞爾吉。在回答你的第一個問題時，即 IgAN 的力量，我們的統計學家相信這一點，並且非常有信心我們被壓倒了。所以我認為我們在那裡狀況良好。是的，我們預計一項 III 期臨床試驗將足以支持 BLA 和 MAA，這與最近獲得批准的其他療法是一致的。所以我們看不出有什麼區別。

With respect to OMIDRIA and HOPD use. Look, we know what happens in the HOPDs. HOPDs represent about 20% of the total procedures. So once we again receive our OMIDRIA again, received separate payment in the HOPDs. We expect to see about a 20% boost in our total revenues or net sales from OMIDRIA at least. And again, I think the key here -- and when I say a 20% boost, I guess that would really be about a 25% increase over where we are given that it's 20% of total net sales.

關於 OMIDRIA 和 HOPD 的使用。看，我們知道 HOPD 中會發生什麼。 HOPD 約佔總手術的 20%。因此，我們再次收到 OMIDRIA，並在 HOPD 中收到單獨付款。我們預計 OMIDRIA 的總收入或淨銷售額至少將增長 20% 左右。再說一次，我認為這裡的關鍵是——當我說增長 20% 時，我想這實際上是比我們假設的增長 25% 左右，因為它佔總淨銷售額的 20%。

I think that the key here is also in the amount of time that we now have secured, so long-term separate payment. How quickly can Rayner lock down Med advantage or Med Part C, separate payment reimbursement. That's the key to this. Because right now, I think still physicians and centers mostly call their patients. They'll look for patients who are Med Part B. And the reason they do that is the concern that if they use OMIDRIA on a Med Part C patient, a Med Advantage patient and are not paid, that is a meaningful cost to them, but there becomes a threshold beyond which if you can access Med Advantage for doesn't need to be 100% of the patients. It just needs to be enough of the patients where physicians and centers then are willing to use it broadly. And once it has that kind of met advantage coverage, then you really -- you don't even need to increase the number of sites or number of customers. You simply are drilling down on those customers on those sites and moving from Med Part B to Med Advantage, which, by definition, then effectively includes commercial because the payers are the same for Med Advantage and commercial.

我認為這裡的關鍵還在於我們現在獲得的時間量，因此長期單獨付款。 Rayner 能多快鎖定 Med 優勢或 Med C 部分（單獨付款報銷）。這是關鍵。因為現在，我認為醫生和中心仍然主要打電話給他們的病人。他們會尋找 Med B 部分患者。他們這樣做的原因是擔心，如果他們對 Med C 部分患者、Med Advantage 患者使用 OMIDRIA 並且沒有得到報酬，這對他們來說是一筆有意義的成本，但存在一個閾值，超過該閾值後，不一定100% 的患者都可以獲得Med Advantage。只需要足夠多的患者，醫生和中心就願意廣泛使用它。一旦它具有這種滿足的優勢覆蓋範圍，那麼您甚至不需要增加站點數量或客戶數量。您只需深入了解這些網站上的客戶，然後從 Med B 部分轉移到 Med Advantage，根據定義，後者實際上包括商業服務，因為 Med Advantage 和商業服務的付款人是相同的。

And all of a sudden, you've opened this up and you've made the drug available to not only Med Part B, but Med Advantage and commercial patients as well, which is really what should happen, right? I mean the drug clearly works. It works well. the benefit-risk ratio is so heavily weighted to the benefit. I know that when we had OMIDRIA, we did not have a single safety signal of concern, 0 associated with the drug. Nothing came to us there. So yes, this is pretty clear but it is really a reimbursement issue. And I think -- I know that Rayner is working on that, and we look forward to their success, which I think will be not only good for Rayner and by extension Omeros. But I think most importantly, it's going to be good for patients. And we need to get that. So let me see Nadia again, anything you want to add to that?

突然間，您打開了這個大門，不僅向 Med Part B 提供了該藥物，還向 Med Advantage 和商業患者提供了該藥物，這確實應該發生，對吧？我的意思是這種藥顯然有效。效果很好。收益風險比對收益的權重如此之大。我知道當我們使用 OMIDRIA 時，我們沒有任何與該藥物相關的安全信號，0。那裡什麼也沒有發生。是的，這很清楚，但這實際上是一個報銷問題。我認為——我知道雷納正在努力解決這個問題，我們期待著他們的成功，我認為這不僅對雷納有利，而且對奧梅羅斯也有利。但我認為最重要的是，這對患者有好處。我們需要做到這一點。讓我再次見到娜迪亞，你還有什麼要補充的嗎？

The only thing I will add, I agree with everything you just said is even going back to the hospital outpatient department question, the request for OMIDRIA continue even without the NOPAIN Act previously. So we know there's demand and there's significant opportunity that we're excited about.

我唯一要補充的是，我同意你剛才所說的一切，甚至回到醫院門診部的問題，即使之前沒有《NOPAIN 法案》，對 OMIDRIA 的要求仍然繼續。所以我們知道有需求，也有令我們興奮的重要機會。

Thank you, Nadia. Yes, I would underscore what Nadia just said. I mean there are a number of HOPDs that are using the product really at their cost because they believe that strongly in it, and they believe that patients should have it. So I think once that HOPD separate payment begins as well, I think it has an amplifying effect across ASCs and HOPDs.

謝謝你，納迪亞。是的，我要強調納迪亞剛才所說的話。我的意思是，有許多 HOPD 確實以自己的成本使用該產品，因為他們堅信該產品，並且他們相信患者應該擁有該產品。因此，我認為一旦 HOPD 單獨付款也開始，我認為它會對 ASC 和 HOPD 產生放大效應。

Our next question comes from the line of Olivia Brayer with Cantor Fitzgerald.

我們的下一個問題來自奧利維亞·布雷耶（Olivia Brayer）和坎托·菲茨杰拉德（Cantor Fitzgerald）的對話。

This is (inaudible) on for Olivia. Could you give us any more color on what type of survival analysis is included in the proposal you're submitting next month for TA-TMA and once you're in agreement with the FDA on those, how quickly do you think you can turn around the survival data for the submission package?

這是奧利維亞（聽不清）的。您能給我們更多關於您下個月提交的 TA-TMA 提案中包含什麼類型的生存分析的信息嗎？一旦您與 FDA 就這些問題達成一致，您認為您能多快扭轉局面提交包的生存數據？

Sure. Thank you. first, with respect to what we are proposing. These are just specific analyses that we think to run that will allow a robust and a meaningful comparison of the survival data from our clinical trial, the TA-TMA trial to survival in the external sources. So there's not really anything magical about this. We just want to submit a detailed proposal so that we hopefully have alignment with FDA. After having done that, submitted that proposal, as I said, this will be part of a Type B meeting, we would expect a response from FDA within 60 days.

當然。謝謝。首先，關於我們的提議。這些只是我們認為要進行的具體分析，可以對我們的臨床試驗（TA-TMA 試驗）的生存數據與外部來源的生存數據進行穩健且有意義的比較。所以這並沒有什麼神奇之處。我們只是想提交一份詳細的提案，以便我們希望與 FDA 保持一致。完成此操作後，提交該提案，正如我所說，這將是 B 類會議的一部分，我們預計 FDA 將在 60 天內做出答复。

Then it is largely for us pushing a button and I don't want to minimize this. I'm sure that our statisticians and data management group might not want me representing it that way. But again, these analyses will already have been set and it is pushing the button, getting the readout. What it will take for us to submit, it's going to be work, but we are resubmitting a BLA. So it's updating safety, it's adding the new information into the BLA and then resubmitting and I think as we said, our objective here is even with the full duration of a 6-month review cycle by FDA. Our objective or our target is to have a decision from FDA in mid 2024. But let me turn to Cathy and see Cathy, what would you like to add to that?

然後這主要是我們按下按鈕，我不想最小化這一點。我確信我們的統計學家和數據管理小組可能不希望我以這種方式表示它。但同樣，這些分析已經被設置，並且正在按下按鈕，獲取讀數。我們需要提交什麼，這將會起作用，但我們正在重新提交 BLA。因此，它正在更新安全性，將新信息添加到 BLA 中，然後重新提交，我認為正如我們所說，我們的目標是在 FDA 6 個月審查週期的整個持續時間內完成。我們的目標是 FDA 在 2024 年中期做出決定。但是讓我轉向 Cathy，Cathy，您想對此補充什麼？

Yes. Only to say that for parts of the resubmission that don't count on the analysis that we still have to do, we are already doing the work and preparing the documents that we need for us. So we're trying to do everything we can sort of in advance and in parallel, so that, as Greg said, we minimize the amount that we need to do once we get the feedback from FDA. So we're working very hard on it right now.

是的。只是說，對於重新提交的部分，我們仍然需要進行分析，我們已經在做工作並準備我們需要的文件。因此，我們正在努力提前並並行地做所有我們能做的事情，這樣，正如格雷格所說，一旦我們得到 FDA 的反饋，我們就可以最大限度地減少我們需要做的事情。所以我們現在正在努力工作。

The objective, of course, on our side, and thanks, Cathy. The objective, of course, is to get the BLA resubmitted as quickly as possible, right? I mean this has been in arduous task, and we want to and expect to get narsoplimab over the finish line in the relatively near term. So we've laid out the time lines. We think that those are reasonable. And I can tell you internally, it's really all hands on deck pushing to get this completed.

目標當然是在我們這邊，謝謝凱茜。當然，目標是盡快重新提交 BLA，對嗎？我的意思是，這是一項艱鉅的任務，我們希望並期望在相對近期內讓 narsoplimab 衝過終點線。所以我們已經制定了時間表。我們認為這些都是合理的。我可以在內部告訴你們，這確實需要所有人齊心協力才能完成。

We had an earlier question about compassionate use. I mean there's clearly a need and a desire for the product. And we get these compassionate use requests, I would say, weekly. I mean we just had -- I think, Cathy, we just had one or more this week already. And when we get those, we don't ask can they pay. We ask particularly if these are children. The question we ask is how quickly can we get it there? How quickly can we get the drug there. So we're trying. We're making this available and we do make it available because we are very confident it works.

我們之前有一個關於同情使用的問題。我的意思是，人們顯然對該產品有需求和渴望。我想說，我們每週都會收到這些富有同情心的使用請求。我的意思是我們剛剛——我想，凱茜，我們這週已經有了一個或多個。當我們得到這些時，我們不會問他們能否付款。我們特別詢問這些人是否是兒童。我們要問的問題是我們能多快到達那裡？我們多久能把藥物送到那裡？所以我們正在努力。我們正在提供此功能，並且確實提供了它，因為我們非常有信心它能發揮作用。

And obviously, the requests that we're getting, I think, indicate the confidence within the transplant community that it works. So our objective as fast as possible, get it over the finish line and make this available broadly to patients, hopefully, adult and pediatric patients make this available so that we can continue to save lives, which I can tell you with complete certainty we're doing right now. Nadia?

顯然，我認為我們收到的請求表明移植界對其有效的信心。因此，我們的目標是盡快越過終點線，並將其廣泛提供給患者，希望成人和兒童患者能夠提供這一服務，以便我們能夠繼續拯救生命，我可以完全肯定地告訴您，我們”現在正在做。納迪亞？

Yes, I'll add something as well in terms of the needs out there and the demand. We've recently attended a couple of payer conferences and continued interactions with the transplant centers. And the #1 question is when are we going to have this because they are eager to have a product that is specifically indicated for TA-TMA. So that they can add it to their formularies, they can get it to patients and not have to deal with off-label use that unfortunately is what is the standard of care and all that's available now. So that is the top question that we have to answer repeatedly.

是的，我還會根據現有的需求和需求添加一些內容。我們最近參加了幾次付款人會議，並繼續與移植中心進行互動。第一個問題是我們什麼時候能擁有這個產品，因為他們渴望擁有專門針對 TA-TMA 的產品。這樣他們就可以將其添加到他們的處方集中，他們可以將其提供給患者，而不必處理標籤外使用，不幸的是，這就是護理標準和現在可用的所有內容。所以這是我們必須反復回答的首要問題。

All right. I hope that answers your question. If not, let us know.

好的。我希望這能回答你的問題。如果沒有，請告訴我們。

And at this time, I'd like to hand the conference back over to Dr. Gregory Demopulos for closing remarks.

此時，我想將會議交回給 Gregory Demopulos 博士做閉幕致辭。

All right. Thank you, operator, and thanks to all of you for joining this morning. As you can see, across our programs, we have a handful of value-driving milestones this quarter and over the next 6 months. All of us at Omeros are looking forward to seeing how they play out. So with that, enjoy the rest of your summer. And as always, we appreciate your continued support. Have a good day.

好的。謝謝接線員，也感謝大家今天早上的加入。正如您所看到的，在我們的所有計劃中，我們在本季度和未來 6 個月內實現了一些價值驅動的里程碑。 Omeros 的所有人都期待著看到他們的表現。就這樣，享受剩下的夏天吧。一如既往，我們感謝您的持續支持。祝你有美好的一天。

This concludes today's conference call. Thank you for your participation. You may now disconnect. Everyone, have a wonderful day.

今天的電話會議到此結束。感謝您的參與。您現在可以斷開連接。祝大家度過美好的一天。