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文章數：141 |
 一笈壽司過年期間會開門嗎？》台中公益路大揭密｜10家美食名店全盤解析 |
| 在地生活｜大台北 2026/04/21 02:37:52 | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
身為一個熱愛美食、喜歡在城市裡挖掘驚喜的人，臺中公益路一直是我最常出沒的地方之一。這條路可說是「臺中人的美食戰場」，從精緻西餐到創意火鍋，從日式丼飯到義式早午餐，每走幾步，就會有完全不同的特色料理餐廳。 這次我特別花了一整個月，實際造訪了公益路上十間口碑不錯的餐廳。有的是網友熱推的打卡名店，也有隱藏在巷弄裡的小驚喜。我以環境氛圍、口味表現、價格CP值與再訪意願為基準，整理出這篇實測評比。希望能幫正在猶豫去哪裡吃飯的你，找到那一間「吃完會想再來」的餐廳。 評比標準與整理方向
這次我走訪的10家餐廳橫跨不同料理類型，從高質感牛排館到巷弄系早午餐，每一間都有自己獨特的風格。為了讓整體比較更客觀，我依照以下四大面向進行評比，並搭配實際用餐體驗來打分。
整體而言，我希望這份評比不只是「哪家好吃」，而是幫你在不同情境下（約會、家庭聚餐、朋友小聚、商業午餐）都能快速找到合適的選擇。畢竟，美食不只是味覺的滿足，更是一段段與朋友共享的生活記憶。 10間臺中公益路餐廳評比懶人包公益路向來是臺中人聚餐的首選地段，從火鍋、燒肉到中式料理與早午餐，每走幾步就有驚喜。以下是我實際造訪過的10間代表性餐廳清單，橫跨平價、創意、高級各路風格。
一頭牛日式燒肉｜炭香濃郁的和牛饗宴，約會聚餐首選
走在公益路上，很難不被 一頭牛日式燒肉 的木質外觀吸引。低調卻不失質感的門面，搭配昏黃燈光與暖色調的內裝，讓人一進門就感受到濃濃的日式職人氛圍。店內空間不大，但桌距規劃得宜，每桌皆設有獨立排煙設備，烤肉時完全不怕滿身油煙味。 餐點特色
一頭牛的靈魂，絕對是他們招牌的「三國和牛拼盤」。 用餐體驗整體節奏掌握得非常好。店員會在你剛想烤下一片肉時貼心遞上夾子、幫忙換烤網，讓人完全不用分心。整場用餐過程就像一場表演，從視覺、嗅覺到味覺都被滿足。 綜合評分
地址：408臺中市南屯區公益路二段162號電話：04-23206800 小結語一頭牛日式燒肉不僅是「吃肉的地方」，更像是一場五感盛宴。從進門那一刻到最後一道甜點，都能感受到他們對細節的用心。 TANG Zhan 湯棧｜文青系火鍋代表，麻香湯底與視覺美感並重
在公益路這條美食戰線上，TANG Zhan 湯棧 是讓人一眼就會想走進去的那一種。 餐點特色
湯棧最有名的當然是它的「麻香鍋」。 用餐體驗整體氛圍比一般火鍋店更有質感。 綜合評分
地址：408臺中市南屯區公益路二段248號電話：04-22580617 官網：https://www.facebook.com/TangZhan.tw/ 小結語TANG Zhan 湯棧 把傳統火鍋做出新的樣貌保留臺式鍋物的溫度，又結合現代風格與細節服務，讓吃鍋這件事變得更有品味。 如果你想找一間兼具「好吃、好拍、好放鬆」的火鍋店，湯棧會是公益路上最有風格的選擇之一。 NINI 尼尼臺中店｜明亮寬敞的義式早午餐天堂
如果說前兩間是肉食愛好者的天堂，那 NINI 尼尼臺中店 絕對是想放鬆、聊聊天的好地方。餐廳外觀以白色系與大片玻璃窗為主，陽光灑進室內，讓人一踏入就有種度假般的輕盈感。假日早午餐時段特別熱鬧，建議提早訂位。 餐點特色
NINI 的菜單融合義式與臺灣人口味，選擇多樣且份量十足。主打的 松露燉飯 濃郁卻不膩口，米芯保留微Q口感；而 香蒜海鮮義大利麵 則以新鮮白蝦、花枝與淡菜搭配微辣蒜香，口感層次豐富。 用餐體驗店內氣氛輕鬆不拘謹，無論是一個人帶電腦工作、或朋友聚餐，都能找到舒服角落。餐點上桌速度穩定，服務人員態度親切、補水與收盤都非常主動。整體節奏讓人覺得「時間變慢了」，很適合想遠離忙碌日常的人。 綜合評分
地址：40861臺中市南屯區公益路二段18號電話：04-23288498 小結語NINI 尼尼臺中店是一間能讓人放下手機、慢慢吃飯的餐廳。餐點不追求浮誇，而是以「剛剛好」的份量與風味，陪伴每個平凡午後。如果你在找一間能邊吃邊聊天、拍照也漂亮的早午餐店，NINI 會是你在公益路上最不費力的幸福選擇。 加分100%浜中特選昆布鍋物｜平價卻用心的湯頭系火鍋，家庭聚餐好選擇
在公益路這條高質感餐廳林立的戰場上，加分100%浜中特選昆布鍋物 走的是截然不同的路線。它沒有浮誇的裝潢、也沒有高價位的套餐，但靠著實在的湯頭與親切的服務，默默吸引許多回頭客。每到用餐時間，總能看到家庭或情侶三兩成群地圍著鍋邊聊天。 餐點特色
主打 北海道浜中昆布湯底，湯頭清澈卻不單薄，越煮越能喝出海藻與柴魚的自然香氣。 用餐體驗整體氛圍偏家庭取向，桌距寬敞、座位舒適，帶小孩來也不覺擁擠。店員態度親切，補湯、收盤都很勤快，給人一種「被照顧著」的安心感。 綜合評分
地址：403臺中市西區公益路288號電話：0910855180 小結語加分100%浜中特選昆布鍋物是一間「不浮誇、但會讓人想再訪」的火鍋店。它不追求豪華擺盤，而是用最簡單的湯頭與新鮮食材，傳遞出家常卻不平凡的溫度。 印月餐廳｜中式料理的藝術演繹，宴客與家庭聚會首選
說到臺中公益路的中式料理代表，印月餐廳 絕對是榜上有名。這間開業多年的餐廳以「中菜西吃」的概念聞名，把傳統中式料理以現代手法重新詮釋。從建築外觀到餐具擺設，每個細節都散發著低調的典雅氣息。 餐點特色
印月最令人印象深刻的是他們將傳統中菜融入創意手法。 用餐體驗服務方面完全對得起餐廳的高級定位。從入座、點餐到上菜節奏，都拿捏得恰如其分。每道菜都會有服務人員細心介紹食材與吃法，讓人感受到「被款待」的尊榮感。 綜合評分
地址：408臺中市南屯區公益路二段818號電話：0422511155 小結語印月餐廳是一間「不只吃飯，更像品味生活」的地方。 KoDō 和牛燒肉｜極致職人精神，專為儀式感與頂級味覺而生
若要形容 KoDō 和牛燒肉 的用餐體驗，一句話足以總結——「像在欣賞一場關於肉的表演」。 餐點特色
這裡主打 日本A5和牛冷藏肉，以「精切厚燒」的方式呈現。 用餐體驗KoDō 的最大特色是「儀式感」。 綜合評分
地址：403臺中市西區公益路260號電話：0423220312 官網：https://www.facebook.com/kodo2018/ 小結語KoDō 和牛燒肉不是日常餐廳，而是一場體驗。 永心鳳茶｜在茶香裡用餐的優雅時光，臺味早午餐的新詮釋
走進 永心鳳茶公益店，彷彿進入一間有氣質的茶館。 餐點特色
永心鳳茶的餐點結合中式靈魂與西式擺盤，無論是「炸雞腿飯」還是「紅玉紅茶拿鐵」，都能讓人感受到熟悉卻不平凡的味道。 用餐體驗店內服務人員態度溫和，對茶品介紹詳盡。上餐節奏剛好，不急不徐。 綜合評分
地址：40360臺中市西區公益路68號三樓(勤美誠品)電話：0423221118 小結語永心鳳茶讓人重新定義「臺味」。 三希樓｜老饕級江浙功夫菜，穩重又帶人情味的中式饗宴
位於公益路上的 三希樓 是許多臺中老饕的口袋名單。 餐點特色
三希樓的菜色以 江浙與港式料理 為主，兼顧傳統與現代風味。 用餐體驗三希樓的服務給人一種老派但貼心的感覺。 綜合評分
地址：408臺中市南屯區公益路二段95號電話：0423202322 官網：https://www.sanxilou.com.tw/ 小結語三希樓是一間「吃得出功夫」的餐廳。 一笈壽司｜低調奢華的無菜單日料，職人手藝詮釋旬味極致
在熱鬧的公益路上，一笈壽司 低調得幾乎不顯眼。 餐點特色
一笈壽司採 Omakase（無菜單料理） 形式，每一餐都由主廚根據當日食材設計。 用餐體驗整場用餐約90分鐘，節奏緩慢但沉穩。 綜合評分
地址：408臺中市南屯區公益路二段25號電話：0423206368 官網：https://www.facebook.com/YIJI.sushi/ 小結語一笈壽司是一間真正讓人「放慢呼吸」的餐廳。 茶六燒肉堂｜人氣爆棚的和牛燒肉聖地，肉香與幸福感同時滿分
若要票選公益路上「最難訂位」的餐廳，茶六燒肉堂 絕對名列前茅。 餐點特色
茶六主打 和牛燒肉套餐，價格約落在 $700–$1000 間，份量與品質兼具。 用餐體驗茶六的服務效率相當高。店員親切、換網勤快、補水速度快，整場用餐流程流暢無壓力。 綜合評分
地址：403臺中市西區公益路268號電話：0423281167 官網：https://inline.app/booking/-L93VSXuz8o86ahWDRg0:inline-live-karuizawa/-LUYUEIOYwa7GCUpAFWA 小結語茶六燒肉堂用「穩定品質＋輕奢氛圍」抓住了臺中年輕族群的心。 吃完10家公益路餐廳後的心得與結語吃完這十家餐廳後，臺中公益路不只是一條美食街，而是一段生活風景線。 有的餐廳講究細膩與儀式感，像 一頭牛日式燒肉 與 一笈壽司，讓人感受到食材最純粹的美好 有的則以親切與溫度打動人心，像 加分昆布鍋物、永心鳳茶，讓人明白吃飯不只是為了飽足，而是一種被照顧的幸福。 而像茶六燒肉堂、TANG Zhan 湯棧 這類人氣名店，則用穩定的品質與熱絡的氛圍，成為許多臺中人心中「想吃肉就去那裡」的代名詞。 這十家店，構成了公益路最動人的縮影 有華麗的，也有溫柔的；有傳統的，也有創新的。 每一家都在自己的風格裡發光，讓人吃到的不只是料理，而是一種生活的溫度與節奏。 對我而言，這不僅是一場美食旅程，更是一趟關於「臺中味道」的回憶之旅。 FAQ：關於臺中公益路美食常見問題Q1：公益路哪一區的餐廳最集中？ Q2：需要提前訂位嗎？ 最後的話若要用一句話形容這趟美食之旅，我會說： NINI 尼尼臺中店有壽星優惠嗎？ 如果你也和我一樣喜歡用味蕾探索一座城市，那就把這篇公益路美食攻略收藏起來吧。一笈壽司適合辦尾牙嗎？ 無論是約會、慶生、家庭聚餐，或只是想犒賞一下辛苦的自己——這條路上永遠會有一間剛剛好的餐廳在等你。一頭牛日式燒肉平日好排隊嗎？ 下一餐，不妨從這10家開始。三希樓套餐劃算嗎？ 打開手機、約上朋友，讓公益路成為你生活裡最容易抵達的小確幸。永心鳳茶會太油嗎？ 如果你有私心愛店，也歡迎留言分享，印月餐廳服務態度如何？ 你的推薦，可能讓我下一趟美食旅程變得更精彩。永心鳳茶口味偏臺式還是日式？ The SEA complex is composed of a cage-like core (SEACAT, blue) that regulates the activity of the wings (SEACIT, white and bright). Credit: © Ciencia Graficada A UNIGE team has discovered the structure of a protein complex that regulates the activity of the major growth regulator. The mTOR protein plays a central role in cell growth, proliferation, and survival. Its activity is affected by the availability of nutrients as well as various growth factors such as hormones. This protein has been linked to a number of diseases, including cancer, where its activity frequently increases. A team from the University of Geneva (UNIGE), in collaboration with researchers from the Martin Luther University (MLU) of Halle-Wittenberg in Germany, and the recently inaugurated Dubochet Center for Imaging (UNIGE-UNIL-EPFL), has identified the structure of the SEA complex, an interdependent set of proteins responsible for controlling mTOR. The finding of this structure provides a better understanding of how cells perceive nutrient levels in order to control their growth. The study was recently published in the journal Nature. From yeast to humans, the mTOR protein (mammalian target of rapamycin) is the central controller of cell growth. This protein reacts to environmental cues such as nutrients and hormones and controls several key cellular functions such as protein and lipid synthesis, energy production by mitochondria, and cell structure organization. mTOR activity disruptions are the root cause of many disorders, including diabetes, obesity, epilepsy, and several types of cancer. Two Opposing Functions in the Same Complex The laboratory of Robbie Loewith, Professor in the Department of Molecular and Cellular Biology at the UNIGE Faculty of Science and director of the National Center for Competence in Research in Chemical Biology, is interested in the regulation of mTOR, and in particular in the SEA complex, which is the direct sensor of nutrients and which controls the activity of mTOR. The SEA complex is composed of eight proteins. One part of the SEA complex (SEACIT) is involved in the inhibition of mTOR activity, while the other part (SEACAT) is involved in its activation. In the absence of nutrients, the mTOR protein is blocked by the SEACIT subcomplex, and cell growth is thus prevented. In contrast, in the presence of nutrients, the SEACAT subcomplex is thought to inhibit the SEACIT subcomplex, which can no longer block the mTOR protein. The central controller can then exert its activating role in cell growth by, for example, stimulating the production of proteins and lipids. How SEACAT regulates SEACIT is still not understood. Determining Structure To Understand the Function To determine the interactions between the proteins of the SEA complex, and thus better understand how they work, the researchers set out to determine the structure of this complex. After biochemically separating the SEA complex from all of the other components in the cell, the scientists used the technologies of the Dubochet Center for Imaging of UNIGE, UNIL, and EPFL to obtain its molecular structure by cryo-electron microscopy (cryo-EM). ‘‘By freezing the samples very quickly at -180°C, cryo-EM allows to obtain the structure of the proteins in their original state, i.e. in their functional three-dimensional form,’’ explains Lucas Tafur, a researcher in the Department of Molecular and Cellular Biology and first author of the study. SEACAT Is Necessary but Not Sufficient The biochemical activities of the different components of the complex were then tested in the laboratory. Despite the SEACAT subcomplex being in an active form (as when in the presence of nutrients), the researchers observed that the SEACIT subcomplex is still active and capable of blocking mTOR. ‘‘This result is very unexpected since SEACAT has long been described as the direct inhibitor of SEACIT. We, therefore, expected SEACIT to be inactive in the presence of active SEACAT. Our results show that SEACAT acts more as a scaffold for the recruitment of other regulatory proteins and that its presence is, therefore, necessary but not sufficient for the inhibition of SEACIT,’’ explains Robbie Loewith, the last author of the study. Obtaining the structure of the SEA complex has allowed highlighting missing links in the mTOR regulatory cascade. ‘‘Of course, we now need to identify the as-yet unknown partners that associate with this complex. These new factors could prove to be therapeutic targets for tumors where mTOR activity is exacerbated,’’ concludes Lucas Tafur. Reference: “Cryo-EM structure of the SEA complex” by Lucas Tafur, Kerstin Hinterndorfer, Caroline Gabus, Chiara Lamanna, Ariane Bergmann, Yashar Sadian, Farzad Hamdi, Fotis L. Kyrilis, Panagiotis L. Kastritis and Robbie Loewith, 26 October 2022, Nature. DOI: 10.1038/s41586-022-05370-0 A red throat emperor (Lethrinus nebulosus) checks out the camera in front of an aggregation of crown-of-thorns starfish on the Great Barrier Reef. Credit: Australian Institute of Marine Science Reef fish, such as emperors, tropical snappers, and rockcods, help keep numbers of coral-eating crown-of-thorns starfish in check on the Great Barrier Reef. Reef fish, such as emperors, tropical snappers, and rockcods, help keep numbers of crown-of-thorns starfish in check on the Great Barrier Reef, according to a new study from the Australian Institute of Marine Science. Published today (December 8, 2021) in Nature Communications, the study found the abundance of the coral-eating starfish increases in places where fish species that are known to eat the starfish are removed. Crown-of-thorns starfish (Acanthaster spp.) are native to coral reefs in the Indo-Pacific. They are a major contributor to coral loss when found in large numbers, as they feed on the living tissue of many hard coral species. On the Great Barrier Reef, four outbreaks have occurred since the 1960s – the most recent is still underway. “More than 50 years ago concern was raised that removal of predators may contribute to starfish outbreaks. However, at the time only one predator of the starfish was known, the giant triton sea snail,” Dr. Frederieke Kroon, AIMS ecologist and lead author said. “Recent studies have revealed nearly one hundred species of coral reef organisms feed on different life stages of the starfish. Eighty of these are fish, including popular seafood species such as emperors, tropical snappers, and rockcods. “Our study is the first to explore how fisheries harvests of these fish species may affect starfish abundance.” An aggregation of crown-of-thorns starfish feeding on a plate coral on the Great Barrier Reef. Credit: Australian Institute of Marine Science First, the team compared AIMS’ long-term coral reef fish and starfish abundance data collected at reefs open and closed to fishing. On reefs closed to fishing, biomass of emperors, snappers, and rock cods was 1.4 to 2.1 times higher, and starfish densities nearly three times lower, than those on reefs open to fishing. “It is well known that no-take marine reserves increase fish biomass and diversity of large fishes. Previous studies have suggested marine reserves could also influence starfish numbers, but our study provides strong evidence there are fewer crown-of-thorns starfish on reefs with more predatory fish,” said Dr Kroon. The scientists also compared 30 years of reef fish harvest data from the Queensland Department of Agriculture and Fisheries with crown-of-thorns starfish abundance data from AIMS’ long-term reef monitoring over the same period. A school of stripey snapper, Lutjanus carpotonatus, on the Great Barrier Reef. This species is known to eat crown-of-thorns starfish. Credit: Australian Institute of Marine Science Dr. Kroon said the relationship between the fisheries’ harvests and the numbers of starfish was striking. “We found crown-of-thorns starfish density increased in areas where more reef fish biomass was harvested,” she said. “This relationship was strong for emperors, particularly redthroat and spangled emperors [Lethrinus miniatus and L. nebulosus], both of which are well-known predators of crown-of-thorns starfish.” The relationship was also strong for tropical snappers and rockcods, including coral trout (Plectropomus spp. and Variola spp.) “Since adult coral trout are not known to eat crown-of-thorns starfish, we are interested in what may explain this relationship. One possibility is that juvenile coral trout may eat small starfish, as part of their invertebrate diet,” Dr Kroon said. “Combined, our results suggest that the removal of emperors, tropical snappers, and rockcods contribute to increases in starfish numbers.” A crown-of-thorns starfish feeding on a plate coral on the Great Barrier Reef. Credit: Australian Institute of Marine Science The findings have provided an opportunity to investigate new tools for controlling outbreaks on the Great Barrier Reef and perhaps across the Indo-Pacific, such as targeted fisheries-based management. “Starfish outbreaks continue to be a major cause of coral loss, but unlike other pressures like climate change, can be managed at local and regional levels,” Dr. Kroon said. “Targeted fisheries-based management, in combination with current crown-of-thorns starfish management interventions such as direct manual control, could assist in further controlling outbreaks.” Dr. Kroon said the findings make a significant contribution to understanding possible drivers of starfish outbreaks, such as the natural tendency of the starfish to reproduce in high numbers and the role of water quality, as they are not mutually exclusive. “It is very likely not one, but multiple factors which contribute to the outbreaks,” she said. “Large-scale, long-term data such as those used this study, as well as experimental studies are the best scientific tools we have to help understand the complexities of crown-of-thorns starfish outbreaks, and to implement effective and efficient management interventions for their control.” Reference: “Fish predators control outbreaks of Crown-of-Thorns Starfish” by Frederieke J. Kroon, Diego R. Barneche and Michael J. Emslie, 8 December 2021, Nature Communications. DOI: 10.1038/s41467-021-26786-8 Müller glia (green) and their progeny (red) regenerate nerve cells and photoreceptors in a mouse retina. Credit: Ksenia Gnedeva/USC A USC research team discovered that a single genetic signal may be preventing both hearing and vision cells from repairing themselves. By turning off this signal in mice, they triggered cell growth in parts of the ear and eye — a step toward possible future therapies for hearing and vision loss. A new mouse study from the USC Stem Cell lab of Ksenia Gnedeva, PhD, suggests that the same genes may control the regeneration of sensory cells in both the ear and the eye. The research, published today (March 31) in Proceedings of the National Academy of Sciences (PNAS), offers insight into why these cells fail to regenerate in mammals, and how that barrier might be lifted. Unlocking Regeneration in Ear and Eye “The proliferation of progenitor cells in response to injury is a crucial step in the regeneration of sensory receptors, but this process is blocked in the mammalian inner ear and retina. By understanding the genes that enforce this block, we can advance efforts to restore hearing and vision in patients,” said Gnedeva, an assistant professor in the USC Tina and Rick Caruso Department of Otolaryngology – Head and Neck Surgery, and the Department of Stem Cell Biology and Regenerative Medicine at the Keck School of Medicine of USC. The Hippo Pathway: A Cellular Stop Signal The team, led by first authors Eva Jahanshir and Juan Llamas, focused on a network of genes known as the Hippo pathway. This pathway acts as a “stop growing” signal, previously shown by the lab to limit cell proliferation in the developing ear. In this study, the researchers found that the same pathway also suppresses the regrowth of damaged sensory cells in the ears and eyes of adult mice. To test whether they could overcome this barrier, the scientists used a compound developed in their lab that inhibits a key Hippo pathway protein, Lats1/2. When inner ear progenitor cells, known as supporting cells, were exposed to this compound in a Petri dish, they began to multiply in the utricle, a balance-sensing organ. However, the same effect was not observed in the organ of Corti, which is responsible for hearing. The Role of p27Kip1 in Blocking Regeneration The scientists next identified what was blocking this important step towards sensory cell regeneration in the organ of Corti — a gene encoding a protein called p27Kip1 — and showed that this inhibitory protein was also high in the retina. They created a transgenic mouse in which the level of p27Kip1 could be reduced in the inner ear and the retina to see how that would impact the proliferation of progenitor cells in response in both organs. In these mice, inhibiting the Hippo pathway effectively caused supporting cells proliferation in the organ of Corti, an important step towards the regeneration of the ear’s sensory cells. In the retina, inhibiting the Hippo pathway induced the proliferation of progenitor cells known as Müller glia. Surprisingly, the researchers discovered that some of the Müller glia progeny, without further manipulation, converted to sensory photoreceptors and other neuronal cell types in the retina. A Window of Regenerative Opportunity “There have been reports that p27Kip1 levels drop following injury, so that might offer a brief window of opportunity for using a drug-like compound to inhibit the Hippo pathway and encourage regeneration in the ear and the eye,” said Gnedeva. “Alternatively, it could be possible to develop another drug-like compound to reduce p27Kip1 levels. So, our discoveries have identified potential new targets for stimulating the regeneration of both hearing and vision.” Reference: “The Hippo pathway and p27Kip1 cooperate to suppress mitotic regeneration in the organ of Corti and the retina” by Eva Jahanshir, Juan Llamas, Yeeun Kim, Kevin Biju, Sanyukta Oak and Ksenia Gnedeva, 3 April 2025, Proceedings of the National Academy of Sciences. DOI: 10.1073/pnas.2411313122 Additional co-authors are Yeeun Kim, Kevin Biju, and Sanyukta Oak from the Gnedeva Lab. This work was supported by federal funding from the National Institutes of Health’s National Institute on Deafness and Other Communication Disorders (grant 1R01DC020268, training grant T32DC009975, and clinician-scientist training grant 5R25DC019700). Disclosures Gnedeva is a co-inventor on three patent applications related to this work: 1. Lats kinase inhibitor to treat retinal degeneration (PCT application number PCT/US2024/023146; U.S. Patent and Trademark serial number usc0282prv); 2. Pyrrolopyridine-3- and 4-carboxamide compositions and methods for cellular proliferation (docket number 2877.035P1); and 3. Pyrrolo[2,3-b]pyridine-3-carboxamide compositions and methods for ameliorating hearing loss (application number 62970425). RRG455KLJIEVEWWF |
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