Abstract: Disclosed are a novel therapeutic means effective and practical against cancer, and a novel substance useful as such a therapeutic means. Provided are novel peptides derived from a partial region of HMGN1, HMGN2, HMGN4 or HMGN5, and anti-cancer agents and anti-cancer effect enhancers containing the peptide as an active ingredient. The peptide of the present invention has an anti-tumor effect even independently, and exerts a remarkably excellent anti-tumor effect particularly when used in combination with an immune checkpoint regulator, or an anti-CD4 antibody or antigen-binding fragment thereof.

Abstract: Disclosed are a novel therapeutic means effective and practical against cancer, and a novel substance useful as such a therapeutic means. Provided are novel peptides derived from a partial region of HMGN1, HMGN2, HMGN4 or HMGN5, and anti-cancer agents and anti-cancer effect enhancers containing the peptide as an active ingredient. The peptide of the present invention has an anti-tumor effect even independently, and exerts a remarkably excellent anti-tumor effect particularly when used in combination with an immune checkpoint regulator, or an anti-CD4 antibody or antigen-binding fragment thereof.

Abstract: Disclosed are a novel therapeutic means effective and practical against cancer, and a novel substance useful as such a therapeutic means. Provided are novel peptides derived from a partial region of HMGN1, HMGN2, HMGN4 or HMGN5, and anti-cancer agents and anti-cancer effect enhancers containing the peptide as an active ingredient. The peptide of the present invention has an anti-tumor effect even independently, and exerts a remarkably excellent anti-tumor effect particularly when used in combination with an immune checkpoint regulator, or an anti-CD4 antibody or antigen-binding fragment thereof.

Abstract: A nucleic acid amplification method using a solid-phase carrier according to the present invention comprises: capturing a target nucleic acid comprising mRNA on a solid-phase carrier; carrying out complementary-strand synthesis on the solid phase; carrying out exonuclease treatment to degrade and remove unreacted target- capturing nucleic acid on the solid phase; and then carrying out mRNA degradation and homopolymer addition by TdT reaction in the presence of a chain-terminating nucleotide triphosphate. According to the method of the present invention, cDNA can be stably and highly efficiently amplified even from a small amount of sample even in cases where the ratio of the amount of enzyme to the DNA substrate on the solid phase is excessive, where the reaction time is excessive, and/or where reagents show lot-to-lot variation.

Abstract: Disclosed is a means for reducing side effects of an immune checkpoint regulator that is used as an anticancer drug or the like. A side-effect reducing agent according to the present invention comprises as an effective ingredient an anti-CD4 antibody having a high cytotoxic activity, or an anti-CD4 antibody or antigen-binding fragment thereof which antibody or fragment comprises a cytotoxic component bound thereto. The anti-CD4 antibody is a human-type chimeric antibody, humanized antibody or human antibody against human CD4. The immune checkpoint regulator may be, for example, an anti-PD-L1 antibody, an antagonistic anti-CTLA-4 antibody, or an agonistic anti-OX40 antibody.

Abstract: Disclosed are a novel therapeutic means effective and practical against cancer, and a novel substance useful as such a therapeutic means. Provided are novel peptides derived from a partial region of HMGN1, HMGN2, HMGN4 or HMGN5, and anti-cancer agents and anti-cancer effect enhancers containing the peptide as an active ingredient. The peptide of the present invention has an anti-tumor effect even independently, and exerts a remarkably excellent anti-tumor effect particularly when used in combination with an immune checkpoint regulator, or an anti-CD4 antibody or antigen-binding fragment thereof.

Abstract: Means that enables monitoring of an anticancer effect of an anti-CD4 antibody or an anticancer drug targeting an immune checkpoint is disclosed. The method for testing a therapeutic effect of a cancer therapy of the present invention is a method for testing a therapeutic effect of an anticancer drug comprising as an effective ingredient an anti-CD4 antibody or an anticancer drug targeting an immune checkpoint, which method comprises investigation of expression of (1) at least one immune checkpoint receptor, (2) CD8, and (3) at least one cell surface molecule selected from the group consisting of CD44 and CD45RO, on T cells using a sample derived from a patient who received the anticancer drug. Induction of a T cell population which is positive for the immune checkpoint molecule (1) and positive for CD8, and which shows high expression of CD44 and/or high expression of CD45RO, indicates that said anticancer drug is producing a therapeutic effect in said patient.

Abstract: Disclosed is a novel means effective for treatment, metastasis-inhibition, and recurrence-inhibition of human solid cancer. A therapeutic agent for solid cancer according to the present invention comprises as an effective ingredient an anti-CD4 antibody having a high cytotoxic activity, or an anti-CD4 antibody or antigen-binding fragment thereof which antibody or fragment comprises a cytotoxic component bound thereto. Said anti-CD4 antibody is a human-type chimeric antibody, humanized antibody or human antibody against human CD4. The therapeutic agent of the present invention produces still higher effects by combined use with antagonist or agonist against immune checkpoint molecule, small molecule anticancer agents, or the like. The therapeutic agent is also effective in suppressing recurrence and metastasis of solid cancer.

Abstract: An object of the present invention is to provide a preventive and/or therapeutic agent for radiation damage that has a novel mechanism of action and can prevent and alleviate a wide range of symptoms of radiation damage for which no therapeutic measures have been available so far, and moreover, is highly safe to humans. A preventive and/or therapeutic agent for radiation damage comprising a compound represented by the following formula (I) such as 5-aminolevulinic acid (5-ALA) or a salt thereof as an active ingredient can be used to improve the survival rate, improve body weight reduction, and alleviate hematopoietic disorder: (wherein R1 represents a hydrogen atom or an acyl group; and R2 represents a hydrogen atom, a linear or branched alkyl group, a cycloalkyl group, an aryl group, or an aralkyl group).

Abstract: Means that enables monitoring of an anticancer effect of an anti-CD4 antibody or an anticancer drug targeting an immune checkpoint is disclosed. The method for testing a therapeutic effect of a cancer therapy of the present invention is a method for testing a therapeutic effect of an anticancer drug comprising as an effective ingredient an anti-CD4 antibody or an anticancer drug targeting an immune checkpoint, which method comprises investigation of expression of (1) at least one immune checkpoint receptor, (2) CD8, and (3) at least one cell surface molecule selected from the group consisting of CD44 and CD45RO, on T cells using a sample derived from a patient who received the anticancer drug. Induction of a T cell population which is positive for the immune checkpoint molecule (1) and positive for CD8, and which shows high expression of CD44 and/or high expression of CD45RO, indicates that said anticancer drug is producing a therapeutic effect in said patient.

Abstract: Disclosed is a novel means effective for treatment, metastasis-inhibition, and recurrence-inhibition of human solid cancer. A therapeutic agent for solid cancer according to the present invention comprises as an effective ingredient an anti-CD4 antibody having a high cytotoxic activity, or an anti-CD4 antibody or antigen-binding fragment thereof which antibody or fragment comprises a cytotoxic component bound thereto. Said anti-CD4 antibody is a human-type chimeric antibody, humanized antibody or human antibody against human CD4. The therapeutic agent of the present invention produces still higher effects by combined use with antagonist or agonist against immune checkpoint molecule, small molecule anticancer agents, or the like. The therapeutic agent is also effective in suppressing recurrence and metastasis of solid cancer.

Abstract: Disclosed is a means for reducing side effects of an immune checkpoint regulator that is used as an anticancer drug or the like. A side-effect reducing agent according to the present invention comprises as an effective ingredient an anti-CD4 antibody having a high cytotoxic activity, or an anti-CD4 antibody or antigen-binding fragment thereof which antibody or fragment comprises a cytotoxic component bound thereto. The anti-CD4 antibody is a human-type chimeric antibody, humanized antibody or human antibody against human CD4. The immune checkpoint regulator may be, for example, an anti-PD-L1 antibody, an antagonistic anti-CTLA-4 antibody, or an agonistic anti-OX40 antibody.

Abstract: The object of the invention is to provide an immunological reconstitution promoter or a prophylactic agent for infections for use in allogeneic hematopoietic stem cell transplantation therapy for tumors. The promoter or prophylactic agent enables the amelioration of delayed immune reconstitution or the prevention of infection following transplantation, while maintaining the GVT effect of allogeneic hematopoietic stem cell transplantation. Specifically, in a transplant patient in whom immune reconstitution is delayed, such reconstitution can be promoted by administering, at an early stage following transplantation, a substance capable of depleting CD4+ cells. Early completion of infection management in the patient and improvement in the survival rate are anticipated as a result. In addition, the risk of complications associated with allogeneic hematopoietic stem cell transplantation is reduced, enabling more widespread use of this therapy.

Abstract: An object of the present invention is to provide a preventive and/or therapeutic agent for radiation damage that has a novel mechanism of action and can prevent and alleviate a wide range of symptoms of radiation damage for which no therapeutic measures have been available so far, and moreover, is highly safe to humans. A preventive and/or therapeutic agent for radiation damage comprising a compound represented by the following formula (I) such as 5-aminolevulinic acid (5-ALA) or a salt thereof as an active ingredient can be used to improve the survival rate, improve body weight reduction, and alleviate hematopoietic disorder: (wherein R1 represents a hydrogen atom or an acyl group; and R2 represents a hydrogen atom, a linear or branched alkyl group, a cycloalkyl group, an aryl group, or an aralkyl group).

Abstract: The object of the invention is to provide an immunological reconstitution promoter or a prophylactic agent for infections for use in allogeneic hematopoietic stem cell transplantation therapy for tumors. The promoter or prophylactic agent enables the amelioration of delayed immune reconstitution or the prevention of infection following transplantation, while maintaining the GVT effect of allogeneic hematopoietic stem cell transplantation. Specifically, in a transplant patient in whom immune reconstitution is delayed, such reconstitution can be promoted by administering, at an early stage following transplantation, a substance capable of depleting CD4+ cells. Early completion of infection management in the patient and improvement in the survival rate are anticipated as a result. In addition, the risk of complications associated with allogeneic hematopoietic stem cell transplantation is reduced, enabling more widespread use of this therapy.

Abstract: The present invention is to provide a method for avoiding specifically and preventively or therapeutically an organ injury in graft-versus host disease (GVHD), a preventive or therapeutic agent therefore, and a method for screening the preventive or therapeutic agent. By inhibiting the interaction between fractalkine and the chemokine receptor CX3CR1 expressed on donor CD8 T cells, and by suppressing specifically organ infiltration by CD8 T cells to intestinal tract and the like, it may be possible to prevent organ injuries in GVHD, and to treat and prevent GVHD selectively. A method using an anti-fractalkine antibody can be exemplified to inhibit the interaction between fractalkine and the chemokine receptor CX3CR1. Moreover, the present invention encompasses a method for screening a substance having a preventive or therapeutic effect on an organ injury in GVHD, that can use a mechanism of the present invention for suppressing organ infiltration by CD8 T cells to intestinal tract or the like.