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  1. What is not clearly seen doesn’t drive our potential customers where we want them.

    #startup #companywebsite #business #customeracquisition #customerbehavior #biochemistry #medicine #inhibitors #science #labwork #proteins #drugtrial #aidrugdiscovery #aimedicine

    -----

    Sign-up link: Newsletter.AndrewLipski.com/

    Short observations about Websites, Apps, Digital Communication, sometimes short Tech News comments.

    Mostly emails under 2 min. read, usually once a week.

  2. What is not clearly seen doesn’t drive our potential customers where we want them.

    #startup #companywebsite #business #customeracquisition #customerbehavior #biochemistry #medicine #inhibitors #science #labwork #proteins #drugtrial #aidrugdiscovery #aimedicine

    -----

    Sign-up link: Newsletter.AndrewLipski.com/

    Short observations about Websites, Apps, Digital Communication, sometimes short Tech News comments.

    Mostly emails under 2 min. read, usually once a week.

  3. What is not clearly seen doesn’t drive our potential customers where we want them.

    #startup #companywebsite #business #customeracquisition #customerbehavior #biochemistry #medicine #inhibitors #science #labwork #proteins #drugtrial #aidrugdiscovery #aimedicine

    -----

    Sign-up link: Newsletter.AndrewLipski.com/

    Short observations about Websites, Apps, Digital Communication, sometimes short Tech News comments.

    Mostly emails under 2 min. read, usually once a week.

  4. What is not clearly seen doesn’t drive our potential customers where we want them.

    #startup #companywebsite #business #customeracquisition #customerbehavior #biochemistry #medicine #inhibitors #science #labwork #proteins #drugtrial #aidrugdiscovery #aimedicine

    -----

    Sign-up link: Newsletter.AndrewLipski.com/

    Short observations about Websites, Apps, Digital Communication, sometimes short Tech News comments.

    Mostly emails under 2 min. read, usually once a week.

  5. European Commission Approves Pfizer’s HYMPAVZI for the Treatment of Adults and Adolescents with Hemophilia A or B With Inhibitors

    Approval in patients ages 12 and older based on Phase 3 data demonstrating superior bleed reduction to on-demand…
    #Europe #EU #EuropeanCommission #factorVIII #FVIII #hemophilia #HYMPAVZI #inhibitors #PfizerInc
    europesays.com/europe/45612/

  6. European Commission Approves Pfizer’s HYMPAVZI for the Treatment of Adults and Adolescents with Hemophilia A or B With Inhibitors

    Approval in patients ages 12 and older based on Phase 3 data demonstrating superior bleed reduction to on-demand…
    #Europe #EU #European #factorVIII #FVIII #hemophilia #HYMPAVZI #inhibitors #PfizerInc
    europesays.com/europe/40680/

  7. europesays.com/ch/39562/ Excellergy to be acquired by Novartis for up to USD 2 billion to advance potentially first-in-class trifunctional effector cell response inhibitors #2 #acquired #advance #be #billion #by #Cell #effector #Excellergy #FirstInClass #for #inhibitors #Novartis #potentially #response #to #trifunctional #Up #usd

  8. When the immune system detects a protein from a pathogen,
    it’s supposed to dispatch killer T cells to eliminate the invader.

    Some cancers can interfere with this process by hijacking the checkpoint proteins that keep our immune system from revving out of control
    and using them to turn T cells off.

    Starting in the mid-1990s, several research teams found success by treating mice with #checkpoint #inhibitors,
    -- then a new class of drugs designed to keep tumor cells from concealing their identity and signaling, effectively, “nothing to see here.”

    Thirty years on, checkpoint inhibitors have become a transformative tool in cancer treatment, especially for melanoma.

    The research that went into developing checkpoint inhibitors showed conclusively that immune cells detect cancer much in the same way they identify other pathogens:

    through differences in protein structure determined by DNA
    —a crucial insight.

    But as revolutionary as checkpoint inhibitors have been for immunotherapy, they don’t work for everyone
    —far from it.

    Some 80 percent of patients do not respond to this class of drugs.

    Researchers are still trying to understand all the mechanisms that play a role in determining who does respond,
    but one key factor is whether the immune system is able to recognize tumor cells on the basis of their mutations.

    This is where mRNA vaccines come in.

    #Jason #Luke, a melanoma researcher who now serves as chief medical officer of mRNA-medicine start-up #Strand #Therapeutics,
    helped to design several ongoing clinical trials of mRNA vaccines for cancer.

    He explains that both checkpoint inhibitors and mRNA vaccines build on our deep evolutionary adaptation for fighting pathogens
    by identifying the proteins they shed in our bodies.

    But checkpoint inhibitors are effective only if the patient’s immune system recognizes the cancer as a threat.

    In contrast, mRNA vaccines have the potential to work even in patients whose cancers haven’t spurred much immune response.

    The trick, Luke says, is using computational tools to decipher which of a given tumor’s mutations are most likely to be found by the immune system.

    #MichaelMemoli
    #WilliamColey #immunotherapy #stroma #MHC

  9. When the immune system detects a protein from a pathogen,
    it’s supposed to dispatch killer T cells to eliminate the invader.

    Some cancers can interfere with this process by hijacking the checkpoint proteins that keep our immune system from revving out of control
    and using them to turn T cells off.

    Starting in the mid-1990s, several research teams found success by treating mice with #checkpoint #inhibitors,
    -- then a new class of drugs designed to keep tumor cells from concealing their identity and signaling, effectively, “nothing to see here.”

    Thirty years on, checkpoint inhibitors have become a transformative tool in cancer treatment, especially for melanoma.

    The research that went into developing checkpoint inhibitors showed conclusively that immune cells detect cancer much in the same way they identify other pathogens:

    through differences in protein structure determined by DNA
    —a crucial insight.

    But as revolutionary as checkpoint inhibitors have been for immunotherapy, they don’t work for everyone
    —far from it.

    Some 80 percent of patients do not respond to this class of drugs.

    Researchers are still trying to understand all the mechanisms that play a role in determining who does respond,
    but one key factor is whether the immune system is able to recognize tumor cells on the basis of their mutations.

    This is where mRNA vaccines come in.

    #Jason #Luke, a melanoma researcher who now serves as chief medical officer of mRNA-medicine start-up #Strand #Therapeutics,
    helped to design several ongoing clinical trials of mRNA vaccines for cancer.

    He explains that both checkpoint inhibitors and mRNA vaccines build on our deep evolutionary adaptation for fighting pathogens
    by identifying the proteins they shed in our bodies.

    But checkpoint inhibitors are effective only if the patient’s immune system recognizes the cancer as a threat.

    In contrast, mRNA vaccines have the potential to work even in patients whose cancers haven’t spurred much immune response.

    The trick, Luke says, is using computational tools to decipher which of a given tumor’s mutations are most likely to be found by the immune system.

    #MichaelMemoli
    #WilliamColey #immunotherapy #stroma #MHC

  10. When the immune system detects a protein from a pathogen,
    it’s supposed to dispatch killer T cells to eliminate the invader.

    Some cancers can interfere with this process by hijacking the checkpoint proteins that keep our immune system from revving out of control
    and using them to turn T cells off.

    Starting in the mid-1990s, several research teams found success by treating mice with #checkpoint #inhibitors,
    -- then a new class of drugs designed to keep tumor cells from concealing their identity and signaling, effectively, “nothing to see here.”

    Thirty years on, checkpoint inhibitors have become a transformative tool in cancer treatment, especially for melanoma.

    The research that went into developing checkpoint inhibitors showed conclusively that immune cells detect cancer much in the same way they identify other pathogens:

    through differences in protein structure determined by DNA
    —a crucial insight.

    But as revolutionary as checkpoint inhibitors have been for immunotherapy, they don’t work for everyone
    —far from it.

    Some 80 percent of patients do not respond to this class of drugs.

    Researchers are still trying to understand all the mechanisms that play a role in determining who does respond,
    but one key factor is whether the immune system is able to recognize tumor cells on the basis of their mutations.

    This is where mRNA vaccines come in.

    #Jason #Luke, a melanoma researcher who now serves as chief medical officer of mRNA-medicine start-up #Strand #Therapeutics,
    helped to design several ongoing clinical trials of mRNA vaccines for cancer.

    He explains that both checkpoint inhibitors and mRNA vaccines build on our deep evolutionary adaptation for fighting pathogens
    by identifying the proteins they shed in our bodies.

    But checkpoint inhibitors are effective only if the patient’s immune system recognizes the cancer as a threat.

    In contrast, mRNA vaccines have the potential to work even in patients whose cancers haven’t spurred much immune response.

    The trick, Luke says, is using computational tools to decipher which of a given tumor’s mutations are most likely to be found by the immune system.

    #MichaelMemoli
    #WilliamColey #immunotherapy #stroma #MHC

  11. When the immune system detects a protein from a pathogen,
    it’s supposed to dispatch killer T cells to eliminate the invader.

    Some cancers can interfere with this process by hijacking the checkpoint proteins that keep our immune system from revving out of control
    and using them to turn T cells off.

    Starting in the mid-1990s, several research teams found success by treating mice with #checkpoint #inhibitors,
    -- then a new class of drugs designed to keep tumor cells from concealing their identity and signaling, effectively, “nothing to see here.”

    Thirty years on, checkpoint inhibitors have become a transformative tool in cancer treatment, especially for melanoma.

    The research that went into developing checkpoint inhibitors showed conclusively that immune cells detect cancer much in the same way they identify other pathogens:

    through differences in protein structure determined by DNA
    —a crucial insight.

    But as revolutionary as checkpoint inhibitors have been for immunotherapy, they don’t work for everyone
    —far from it.

    Some 80 percent of patients do not respond to this class of drugs.

    Researchers are still trying to understand all the mechanisms that play a role in determining who does respond,
    but one key factor is whether the immune system is able to recognize tumor cells on the basis of their mutations.

    This is where mRNA vaccines come in.

    #Jason #Luke, a melanoma researcher who now serves as chief medical officer of mRNA-medicine start-up #Strand #Therapeutics,
    helped to design several ongoing clinical trials of mRNA vaccines for cancer.

    He explains that both checkpoint inhibitors and mRNA vaccines build on our deep evolutionary adaptation for fighting pathogens
    by identifying the proteins they shed in our bodies.

    But checkpoint inhibitors are effective only if the patient’s immune system recognizes the cancer as a threat.

    In contrast, mRNA vaccines have the potential to work even in patients whose cancers haven’t spurred much immune response.

    The trick, Luke says, is using computational tools to decipher which of a given tumor’s mutations are most likely to be found by the immune system.

    #MichaelMemoli
    #WilliamColey #immunotherapy #stroma #MHC

  12. When the immune system detects a protein from a pathogen,
    it’s supposed to dispatch killer T cells to eliminate the invader.

    Some cancers can interfere with this process by hijacking the checkpoint proteins that keep our immune system from revving out of control
    and using them to turn T cells off.

    Starting in the mid-1990s, several research teams found success by treating mice with #checkpoint #inhibitors,
    -- then a new class of drugs designed to keep tumor cells from concealing their identity and signaling, effectively, “nothing to see here.”

    Thirty years on, checkpoint inhibitors have become a transformative tool in cancer treatment, especially for melanoma.

    The research that went into developing checkpoint inhibitors showed conclusively that immune cells detect cancer much in the same way they identify other pathogens:

    through differences in protein structure determined by DNA
    —a crucial insight.

    But as revolutionary as checkpoint inhibitors have been for immunotherapy, they don’t work for everyone
    —far from it.

    Some 80 percent of patients do not respond to this class of drugs.

    Researchers are still trying to understand all the mechanisms that play a role in determining who does respond,
    but one key factor is whether the immune system is able to recognize tumor cells on the basis of their mutations.

    This is where mRNA vaccines come in.

    #Jason #Luke, a melanoma researcher who now serves as chief medical officer of mRNA-medicine start-up #Strand #Therapeutics,
    helped to design several ongoing clinical trials of mRNA vaccines for cancer.

    He explains that both checkpoint inhibitors and mRNA vaccines build on our deep evolutionary adaptation for fighting pathogens
    by identifying the proteins they shed in our bodies.

    But checkpoint inhibitors are effective only if the patient’s immune system recognizes the cancer as a threat.

    In contrast, mRNA vaccines have the potential to work even in patients whose cancers haven’t spurred much immune response.

    The trick, Luke says, is using computational tools to decipher which of a given tumor’s mutations are most likely to be found by the immune system.

    #MichaelMemoli
    #WilliamColey #immunotherapy #stroma #MHC

  13. KRAS Inhibitors: Targeting the 'Undruggable' Mutation in 2026 and Beyond Once deemed "undruggable" due to its smooth surface and high affinity for GTP, the KRAS oncogene has become ...

    #cancer #KRAS #inhibitors #pharma

    Origin | Interest | Match
  14. KRAS Inhibitors: Targeting the 'Undruggable' Mutation in 2026 and Beyond Once deemed "undruggable" due to its smooth surface and high affinity for GTP, the KRAS oncogene has become ...

    #cancer #KRAS #inhibitors #pharma

    Origin | Interest | Match
  15. KRAS Inhibitors: Targeting the 'Undruggable' Mutation in 2025 and Beyond Once deemed "undruggable" due to its smooth surface and high affinity for GTP, the KRAS oncogene has become ...

    #cancer #KRAS #inhibitors #pharma

    Origin | Interest | Match
  16. KRAS Inhibitors: Targeting the 'Undruggable' Mutation in 2025 and Beyond Once deemed "undruggable" due to its smooth surface and high affinity for GTP, the KRAS oncogene has become ...

    #cancer #KRAS #inhibitors #pharma

    Origin | Interest | Match
  17. KRAS Inhibitors: Targeting the 'Undruggable' Mutation in 2025 and Beyond Once deemed "undruggable" due to its smooth surface and high affinity for GTP, the KRAS oncogene has become ...

    #cancer #KRAS #inhibitors #pharma

    Origin | Interest | Match
  18. Effects of #JAK #inhibitors in adults admitted to #hospital due to #COVID19: a systematic review and individual participant data meta-analysis of randomised clinical trials, etidiohnew.blogspot.com/2025/0

  19. Effects of #JAK #inhibitors in adults admitted to #hospital due to #COVID19: a systematic review and individual participant data meta-analysis of randomised clinical trials, etidiohnew.blogspot.com/2025/0

  20. Effects of #JAK #inhibitors in adults admitted to #hospital due to #COVID19: a systematic review and individual participant data meta-analysis of randomised clinical trials, etidiohnew.blogspot.com/2025/0

  21. Effects of #JAK #inhibitors in adults admitted to #hospital due to #COVID19: a systematic review and individual participant data meta-analysis of randomised clinical trials, etidiohnew.blogspot.com/2025/0

  22. Effects of #JAK #inhibitors in adults admitted to #hospital due to #COVID19: a systematic review and individual participant data meta-analysis of randomised clinical trials, etidiohnew.blogspot.com/2025/0

  23. Great keynote lecture by Marta Artola of the @LED3hub at #Lunteren. She talked about the importance of glycosidases in various diseases and her great work on conformationally locked #covalent and non-covalent #inhibitors and #probes.
    #chemistry #ChemBio
    pubs.acs.org/doi/10.1021/jacs.

  24. Great keynote lecture by Marta Artola of the @LED3hub at #Lunteren. She talked about the importance of glycosidases in various diseases and her great work on conformationally locked #covalent and non-covalent #inhibitors and #probes.
    #chemistry #ChemBio
    pubs.acs.org/doi/10.1021/jacs.

  25. Great keynote lecture by Marta Artola of the @LED3hub at #Lunteren. She talked about the importance of glycosidases in various diseases and her great work on conformationally locked #covalent and non-covalent #inhibitors and #probes.
    #chemistry #ChemBio
    pubs.acs.org/doi/10.1021/jacs.

  26. #Structural and #virologic #mechanism of the emergence of #resistance to #Mpro #inhibitors in #SARS-CoV-2, PNAS: pnas.org/doi/abs/10.1073/pnas.

    We generated SARS-CoV-2 variants resistant to three SARS-CoV-2 main protease (Mpro) inhibitors (#nirmatrelvir, TKB245, and 5h), by propagating the ancestral SARS-CoV-2WK521WT in VeroE6TMPRSS2 cells with increasing concentrations of each inhibitor and examined their structural and virologic profiles.

  27. #Structural and #virologic #mechanism of the emergence of #resistance to #Mpro #inhibitors in #SARS-CoV-2, PNAS: pnas.org/doi/abs/10.1073/pnas.

    We generated SARS-CoV-2 variants resistant to three SARS-CoV-2 main protease (Mpro) inhibitors (#nirmatrelvir, TKB245, and 5h), by propagating the ancestral SARS-CoV-2WK521WT in VeroE6TMPRSS2 cells with increasing concentrations of each inhibitor and examined their structural and virologic profiles.

  28. #Structural and #virologic #mechanism of the emergence of #resistance to #Mpro #inhibitors in #SARS-CoV-2, PNAS: pnas.org/doi/abs/10.1073/pnas.

    We generated SARS-CoV-2 variants resistant to three SARS-CoV-2 main protease (Mpro) inhibitors (#nirmatrelvir, TKB245, and 5h), by propagating the ancestral SARS-CoV-2WK521WT in VeroE6TMPRSS2 cells with increasing concentrations of each inhibitor and examined their structural and virologic profiles.

  29. #Structural and #virologic #mechanism of the emergence of #resistance to #Mpro #inhibitors in #SARS-CoV-2, PNAS: pnas.org/doi/abs/10.1073/pnas.

    We generated SARS-CoV-2 variants resistant to three SARS-CoV-2 main protease (Mpro) inhibitors (#nirmatrelvir, TKB245, and 5h), by propagating the ancestral SARS-CoV-2WK521WT in VeroE6TMPRSS2 cells with increasing concentrations of each inhibitor and examined their structural and virologic profiles.

  30. #Structural and #virologic #mechanism of the emergence of #resistance to #Mpro #inhibitors in #SARS-CoV-2, PNAS: pnas.org/doi/abs/10.1073/pnas.

    We generated SARS-CoV-2 variants resistant to three SARS-CoV-2 main protease (Mpro) inhibitors (#nirmatrelvir, TKB245, and 5h), by propagating the ancestral SARS-CoV-2WK521WT in VeroE6TMPRSS2 cells with increasing concentrations of each inhibitor and examined their structural and virologic profiles.