From Tylenol to Opium

Korea version | 한국말 버젼
살면서 가끔 이런 생각을 한다.
만약 이 세상에 타이레놀이 없다면, 나는 아이를 어떻게 키웠을까, 끼울까?
열이 나고, 밤새 힘들었던 순간들. 부모라면 누구나 타이레놀의 경이에 의지해 본 경험이 있을 것이다.

우리는 익숙하게 타이레놀을 사용하지만, 타이레놀의 역사는 언제 시작된 것일까?

타이레놀의 긴 역사
많은 사람들이 타이레놀을 현대 의약품이라고 생각하지만, 그 역사는 생각보다 길다.
1955년 미국 McNeil Laboratories는 Tylenol이라는 이름으로 어린이용 해열제를 출시했다. 이후 1959년 Johnson & Johnson이 회사를 인수하면서 타이레놀은 미국 전역으로 보급되었고, 오늘날 가장 널리 사용되는 진통·해열제 중 하나가 되었다. 하지만 아세트아미노펜 자체는 훨씬 오래전인 1878년 미국 화학자 Harmon Northrop Morse에 의해 처음 합성되었다.
1890년대부터 진통과 해열 목적으로 사용되기 시작했지만, 당시에는 이미 의학계를 지배하고 있던 더 강력한 약물이 있었다. 바로 아편(Opium)이다.

인류와 함께한 진통제, 아편
아편은 인류가 수천 년 동안 사용해 온 천연 진통제이자 만병통치약이었다.
양귀비에서 얻어지는 이 물질은 통증을 줄이는 놀라운 효과를 가지고 있다.하지만 문제는 진통 효과만큼이나 강력한 의존성 중독성이다.

19세기 초 독일의 젊은 화학 견습생 Friedrich Sertürner는 아편 속에서 가장 강력한 활성 성분을 분리하는 데 성공한다. 그는 이 물질에 꿈의 신 Morpheus의 이름을 따서 Morphine이라는 이름을 붙였다. 당시 그는 자신에게 직접 약물을 투여하며 실험했고, 훗날 이 물질이 위험할 수 있다는 강력한 경고를 남긴다. 그러나 의학계는 모르핀의 강력한 진통 효과에 매료되었다.
1827년 Merck가 대량생산을 시작하면서 모르핀은 전 세계 의료 현장으로 빠르게 퍼졌다.

더 강한 약을 향한 욕망
1853년 스코틀랜드 의사 Alexander Wood는 주사기를 이용해 모르핀을 직접 체내에 주입하면 더 적은 양으로 효과를 낼 수 있다고 생각했다. 그 결과 모르핀 주사는 빠르게 확산되었다. 그 첫번째 약물과다 복용의 희생량은 Wood의 부인이었다.

당시 의사들은 더 강력하면서도 중독성이 적은 진통제를 찾았다. 그리고 그 과정에서 탄생한 것이 Heroin (acetylated morphine)이었다. 1898년 Bayer는 모르핀을 화학적으로 변형한 약물을 Heroin이라는 이름으로 판매하기 시작했다. 그 당신 관련 연구자들은 이 약물이 모르핀보다 안전하고 중독성이 적을 것이라는 성급한 결론을 내렸다. 하지만 그것은 치명적인 오판이었다. 헤로인은 더 빠르게 뇌에 도달했고, 더 강한 쾌감과 의존성을 만들었다. 20세기 초가 되자 의사들과 연구자들은 헤로인의 위험성을 인식하기 시작했고, 미국은 1924년 Heroin Act를 통해 헤로인의 제조와 판매를 금지한다.

Natural은 Safe를 의미하지 않는다
흥미로운 점은 모르핀, 헤로인, 그리고 현대의 오피오이드 진통제들이 모두 자연에서 시작되었다는 사실이다.
양귀비는 아름다운 꽃이다. 어떤 사람은 꽃이 아름답다고 말하고, 어떤 사람은 향기가 좋다고 말한다. 하지만 그 아름다운 꽃은 동시에 인류 역사상 가장 강력한 진통제와 가장 심각한 약물 의존 문제를 만들어낸 출발점이다.

우리는 종종 "천연 성분"이라는 말을 들으면 안전하다고 생각하고 상업적으로 이용된다. 그러나 역사는 그렇지 않다고 말한다. 독버섯도 천연이고, 아편도 천연이다. Natural과 Safe는 결코 같은 의미가 아니다.

타이레놀에서 다시 시작된 질문
아마 그래서 합성의약품인 타이레놀이 더 흥미로운지도 모른다.
오늘날 수많은 부모들이 아이의 열을 내리기 위해 사용하는 비교적 안전한 약. 이 약은 안전하지만, 시럽을 물처럼 마시면 물론 안 된다. 간에 치명적인 해로움을 끼칠 수 있다.
100년 넘게 사용되어 왔지만 아직도 작용기전이 완전히 밝혀지지 않은 약 (아무래도 열을 낮춘다는 것 자체가 면역작용을 통제하고, 그 결과가 우회적으로 아픔을 통제할 것같다).
그리고 무엇보다 아편이나 모르핀과는 전혀 다른 길을 걸어온 진통제.

진통제의 역사를 돌아보면, 그것은 단순한 의학의 발전사가 아니다.

인간의 고통을 줄이려는 노력과 과학적 호기심, 때로는 성급한 결론, 그리고 상업적 이해관계가 끊임없이 교차하고 있는 역사이다.

타이레놀에서 시작된 오늘의 글은… 야산의 양귀비 꽃 (지금 이시대에는 야산에 양귀비 꽃은 없겠지만..)으로 이어졌다. 난 실재로 양귀비 꽃에 대해 초등학교 수업 때 들은 적은 있어도 본 적은 없다.

Sometimes I find myself wondering: if Tylenol had never existed, how would I have raised my children?

The fevers, the countless nights spent comforting a restless child who couldn’t sleep. Almost every parent has probably relied on Tylenol at some point.

We use Tylenol so routinely today that we rarely stop to think about it. But when did the history of pain relief actually begin?

The Long History of Tylenol

Many people think of Tylenol as a modern medicine, but its history is much longer than most realize.

In 1955, McNeil Laboratories introduced a children’s fever reducer under the brand name Tylenol. After Johnson & Johnson acquired the company in 1959, Tylenol became widely available across the United States and eventually grew into one of the most commonly used pain relievers and fever reducers in the world.

Acetaminophen itself, however, dates back much further. It was first synthesized in 1878 by the American🇺🇸 chemist Harmon Northrop Morse. By the 1890s, it was already being used to relieve pain and reduce fever. Yet at the time, medicine was dominated by a much more powerful substance. That substance was opium.

Opium: The Painkiller That Accompanied Human History

Opium is a natural pain reliever that humans have used for thousands of years.

Derived from the opium poppy, it possesses remarkable pain-relieving properties. The problem, however, is that its power to relieve pain is matched by its ability to create dependence.

In the early nineteenth century, a young German🇩🇪 chemical apprentice named Friedrich Sertürner succeeded in isolating the most potent active ingredient found in opium. He named the substance Morphine after Morpheus, the Greek god of dreams.

Like many early scientists, Sertürner experimented on himself. He administered the substance to his own body and later warned that it could be dangerous. Nevertheless, the medical community was captivated by morphine’s extraordinary ability to relieve pain.

When Merck began mass-producing morphine in 1827, it rapidly spread throughout medical practice around the world.

The Desire for a Stronger Drug

In 1853, the Scottish🏴󠁧󠁢󠁳󠁣󠁴󠁿 physician Alexander Wood believed that injecting morphine directly into the body would allow doctors to achieve the same effects with smaller doses. As a result, injectable morphine quickly gained popularity and The first victim of the injected morphine was Wood’s wife.

At the same time, physicians continued searching for a painkiller that was even more effective while being less addictive.

Out of that research came heroin, acetylated morphine.

In 1898, Bayer began marketing a chemically modified form of morphine under the name Heroin.

Early researchers hoped that this new drug would be safer and less addictive than morphine. It was a devastating miscalculation.

Heroin reached the brain more rapidly, produced stronger feelings of euphoria, and ultimately proved even more addictive. By the early twentieth century, doctors and researchers had begun recognizing its dangers. In 1924, the United States passed the Heroin Act, effectively banning the manufacture and sale of heroin.

Natural Does Not Mean Safe

One of the most interesting aspects of this story is that morphine, heroin, and modern opioid painkillers all originated from nature.

The poppy is a beautiful flower. Some people admire its appearance. Others appreciate its fragrance. Yet this beautiful flower also became the starting point for some of the most powerful pain-relieving drugs and some of the most devastating addiction problems in human history.

We often assume that something described as “natural” must also be safe. History tells a different story.

Poisonous mushrooms are natural. Opium is natural. Natural and safe are not the same thing.

A Question That Returns to Tylenol

Perhaps that is one reason why Tylenol, a synthetic drug, remains so fascinating.

It is the medicine countless parents use to bring down a child’s fever. Of course, while this medication is safe, you certainly must not drink the syrup as if it were water. Doing so could cause fatal harm to your liver.

It has been used for well over a century, yet its precise mechanism of action is still not completely understood. (It seems that lowering a fever essentially regulates the immune response, and that this, in turn, indirectly helps control the pain.)

Most importantly, it followed a path very different from that of opium or morphine🪜.

When we look back at the history of painkillers, we are looking at more than the history of medicine.

It is also the story of humanity’s effort to reduce suffering, a story shaped by scientific curiosity, occasional premature conclusions, and powerful commercial interests 🤑.

Today’s reflections began with Tylenol, but somehow led me all the way to the poppy flower 🌺.

Growing up, I heard about poppies in elementary school, but I have never actually seen one in person. Perhaps wild opium poppies once existed in fields and hillsides somewhere in Korea, but certainly not today.

Personalized gene-editing

KJ Muldoon (infant) is the first person in the world who received  in vivo gene-editing therapy making medical history in 2025. It was made at Children’s Hospital of Philadelphia/Penn Medicine. 

KJ was born with a rare metabolic disorder known as severe carbamoyl phosphate synthetase 1 (CPS1) deficiency, a life-threatening metabolic disorder that impairs the body’s ability to clear ammonia. 

Genetic analysis revealed that KJ inherited two distinct truncating (nonsense premature stop) variants in the CPS1 gene: Q335X (it means Glutamine into Stop codon at the site of CDS 335) and E714X (glutamic acid into stop codon at CDS 714). If you want to see the variant details about this mutation, click here:

A team led by Drs. Rebecca Ahrens-Nicklas and Kiran Musunuru developed a therapy delivered via lipid nanoparticles to the liver that uses a base-editing CRISPR. The first dose was administered in February 2025 (at 6-7 months old) and followed by further escalating doses in March and April (7-8 months old). 

The team chose to target one of the two mutants (rather than both), and selected the Q335X variant for the adenine base editing (A—>G conversion). Maybe this is a good strategy because of off-targets and bystand targets.

Doctors reported that the treatment was successful in correcting the genetic defect and reducing ammonia levels in KJ’s blood. He was able to go home from the hospital in June 2025 and is currently thriving. 

We do not know editing efficiency, off-target and by-stand target rate, but saved a life. 

For more detailed news, please click here

(biotech news) Personalized CRISPR startup, Aurora, Jan 9 2026

Antibodies: From Lab Bench to Therapeutic Drugs

I’ve always been fascinated by antibodies. My journey began in 2000, when I first took an undergraduate immunology class. During graduate school in Medical Biotechnology, I dove deeper—advanced immunology in 2001, psychoneuroimmunology in 2002—researching NKT cells and CD1d in autoimmune diseases. Back then, my curiosity was pure: I just wanted to understand how things worked. Papers, grants, and impact factors? I didn’t think about those. Honestly, even now, grant writing still feels like a mountain to climb!

Until 2018, during my third postdoc, I never actively pursued grants. I was fortunate to be in well-funded labs, free to follow my interests, attend meetings, and write papers when inspiration struck. That freedom was exhilarating. I often chose research topics my supervisors weren’t interested in—at least initially—giving me the joy of discovery.

But freedom has a cost. By the time I tried to apply for my own grant, it felt late. I wrote one in 2018, only to have my name removed by my PIs and replaced with a colleague’s. They told me it would increase our chances of funding. I also learned a hard lesson: in both academia and industry, even great data isn’t always shareable due to patents. At the end of the day, the only guaranteed rewards were a paycheck and the sheer pleasure of exploring science.

Sometimes I wonder if I should have pursued a Ph.D. in immunology instead of neurobiology. I missed a lot of immunology along the way. Still, I wouldn’t trade my journey—it shaped the scientist I am today.


Generating Antibodies: My Hands-On Experience

If you’ve worked in biology or medicine, you know antibodies are everywhere. They’re essential for research and diagnostics, from simple antibody staining to generating completely new reagents.

During my Ph.D., I generated antibodies both in-house and through companies. I provided expression constructs, sometimes purified proteins, and worked with animals like mice or ferrets. It took time, patience, and more than a few failed attempts—especially for antibodies against certain domains. For instance, when generating pan-antibodies against protocadherin 7, we eventually produced polyclonal antibodies, but monoclonal antibodies just didn’t cooperate.

Fast forward to 2020–2021: antibody engineering has advanced tremendously. I created numerous AAV constructs, including Fab and scFv, analyzing backbones, VH, VL, CDRs in detail. Companies sometimes tweaked CDRs sequences, either randomly or with AI. Even Fc regions required careful attention, as they could influence adverse effects in the case of Fc-fused proteins and full antibody drugs. To generate AAV constructs, all other parts, such as promoter regions, signal peptides, linkers, polyA, WPRE, etc., should be considered. The next steps are to check whether the antibody-based fragments are secreted and work properly by Western blots and ELISA. Of course, in the case of AAV constructs, we should check AAV property and yields and have AAV first.


Fc and Fab: The Power of Two

Antibodies have two main regions: Fab and Fc.

  • Fab or variable regions bind to antigens
  • Fc, often called the “effector arm or tail,” performs critical functions:
    1. Cell-mediated and humoral immune activation: Fc binds Fc receptors on macrophages, neutrophils, NK cells, and dendritic cells and leads to ADCC (antibody-dependent cellular cytotoxicity) and ADCP (antibody-dependent cellular phagocytosis).
    2. Complement system activation: Fc triggers pathogen lysis, opsonization, and inflammation.
    3. Half-life regulation: Fc binds neonatal Fc receptor (FcRn) in endothelial cells, protecting antibodies from degradation.
    4. Maternal-fetal transfer: IgG Fc interacts with FcRn in the placenta, passing immunity to the fetus.

When designing therapeutic antibodies, deciding whether to keep, engineer, or remove Fc is crucial. Fab fragments penetrate tissues better but have shorter half-lives. Fc is often necessary for cancer therapies, whereas autoimmune or blocking therapeutics benefit from Fc engineering to avoid harming self-tissues.


A Look at Therapeutic Antibodies

Here’s an overview of some major monoclonal antibody drugs and their Fc strategies:

DrugTargetIndicationFc StrategyEngineering / Mutations
RituximabCD20B-cell lymphoma, RAActive Fc → ADCC + CDCNone
TrastuzumabHER2HER2+ breast & gastric cancerActive Fc → ADCCNone
AdalimumabTNF-αRA, Crohn’s, psoriasisNeutralizingNone
CetuximabEGFRColorectal & head/neck cancerActive Fc → ADCCNone
NivolumabPD-1Melanoma, NSCLCFc-silent → avoids killing T cellsIgG4 backbone + S228P
PembrolizumabPD-1SimilarFc-silentIgG4 backbone + S228P
OmalizumabIgESevere asthma, urticariaFc engineered to avoid mast cell activationIgG1 backbone; avoids C1q binding
BevacizumabVEGF-AColorectal cancer, AMDNeutralizing; Fc not criticalWild-type IgG1

Key patterns:

  • Cancer drugs keep Fc active to kill tumor cells.
  • Checkpoint inhibitors silence Fc to avoid killing PD-1+ T cells.
  • Anti-cytokine drugs have no effector function, but increase half-life by FcRn recycling.
  • Anti-IgE drugs engineer Fc to prevent dangerous immune activation.

Fc-Free Antibodies: A Growing Field

Fc-free antibody fragments are also gaining attention. As of August 27, 2025:

StatusCount%
FDA-approved1527%
Terminated / Withdrawn1018%
Under Clinical Development2647%
Regulatory review47%
database for Therapeutic Antibodies (db.antibodysociety.org)

Even though Fc can trigger strong immune responses, careful control – through dosing or engineering – can make it highly beneficial. Fc-free fragments face challenges like short half-life or lack of effector function, explaining why some have been terminated.


Antibody research is a perfect blend of biology, engineering, and clinical innovation. It’s a field full of stories – both successes and failures – that teach us how to translate basic science into therapies. 

I’ve recently started reading again a book on therapeutic antibody engineering (2012), and I plan to share insights and reflections here from time to time.

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